gastrins and Peptic-Ulcer

Topics: Animals; Disease Models, Animal; Gastrins; Gastrointestinal Diseases; Gastrointestinal Neoplasms; Humans; Pancreas; Peptic Ulcer; Protein Precursors

The hormone gastrin plays 2 important roles in gastrointestinal physiology--1 as a major factor in meal-stimulated gastric acid secretion and the other as a trophic hormone for epithelial and enterochromaffin cells. These roles are exaggerated to the point of pathology under conditions of chronic hypergastrinemia as exemplified by the Zollinger-Ellison syndrome and pernicious anemia. More recently, the concern about the potential risk of chronic hypergastrinemia has risen because of the widespread use of proton pump inhibitors for maintenance therapy in reflux esophagitis. For this reason, we present a concise overview of the origin, causes, and potential risks of chronic hypergastrinemia.

Topics: Animals; Enzyme Inhibitors; Gastric Acid; Gastrinoma; Gastrins; Gastritis, Atrophic; Humans; Peptic Ulcer; Proton Pump Inhibitors; Risk Factors; Zollinger-Ellison Syndrome

Proton pump inhibitors are being increasingly used and for longer periods of time, especially in patients with gastroesophageal reflux disease. Each of these trends has led to numerous studies and reviews of the potential risk-benefit ratio of the long-term use of proton pump inhibitors. Both long-term effects of hypergastrinaemia due to the profound acid suppression caused by proton pump inhibitors as well as the effects of hypo-/achlorhydria per se have been raised and studied. Potential areas of concern that have been raised in the long-term use of proton pump inhibitors, which could alter this risk-benefit ratio include: gastric carcinoid formation; the development of rebound acid hypersecretion when proton pump inhibitor treatment is stopped; the development of tolerance; increased oxyntic gastritis in H. pylori patients and the possibility of increasing the risk of gastric cancer; the possible stimulation of growth of non-gastric tumours due to hypergastrinaemia; and the possible effect of the hypo/achlorhydria on nutrient absorption, particularly iron and vitamin B12. Because few patients with idiopathic gastro-oesophageal reflux disease/peptic ulcer disease have been treated long-term (i.e., >10 years), there is little known to address the above areas of potential concern. Most patients with gastrinomas with Zollinger-Ellison syndrome have life-long hypergastrinaemia, require continuous proton pump inhibitors treatment and a number of studies report results of >5-10 years of tratment and follow-up. Therefore, an analysis of Zollinger-Ellison syndrome patients can provide important insights into some of the safety concerns raised above. In this paper, results from studies of Zollinger-Ellison syndrome patients and other recent studies dealing with the safety concerns above, are briefly reviewed.

Topics: Animals; Carcinoid Tumor; Cell Transformation, Neoplastic; Drug Tolerance; Enterochromaffin-like Cells; Gastric Acid; Gastric Mucosa; Gastrinoma; Gastrins; Gastritis; Gastroesophageal Reflux; Gastrointestinal Agents; Helicobacter pylori; Humans; Malabsorption Syndromes; Peptic Ulcer; Proton Pump Inhibitors; Stomach Neoplasms; Time Factors; Zollinger-Ellison Syndrome

To commemorate Edkins' discovery of gastrin in 1905, we review a century of progress in the physiology and pathobiology of gastrin and acid secretion especially as it pertains to clinical aspects of gastro-oesophageal reflux disease. Although initially ignored, Edkins' observations eventually led to the enthusiastic investigation of gastrin and acid regulation in peptic ulcer disease, culminating in important therapeutic advances in the management of acid peptic disease. Following the improved understanding of gastric secretory physiology, and the development of acid suppressants with increasing efficacy, the use of surgical intervention for peptic ulcer disease was almost eliminated. Surgery became obsolete with the discovery of Helicobacter pylori. Three other advances are also influencing modern practice: the gastrotoxicity of aspirin and non-steroidal anti-inflammatory drugs is now increasingly appreciated, the role of endoscopy in the diagnosis and therapy of upper gastrointestinal bleeding, and the use of intravenous acid-suppressive agents. The major issue for the future resides within the epidemic of gastro-oesophageal reflux disease. How to diagnose, categorize and treat this condition and how to identify and prevent neoplasia, are the challenges of the new century.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Endoscopy, Gastrointestinal; Gastrins; Gastroesophageal Reflux; Helicobacter Infections; Helicobacter pylori; Histamine H2 Antagonists; Humans; Peptic Ulcer; Peptic Ulcer Hemorrhage; Proton Pump Inhibitors

Aphton is developing an anti-gastrin vaccine [Anti-gastrin 17 immunogen, G17DT, Gastrimmune], which neutralises the gastrin 17 hormone and the Gly-G17 hormone. Gastrin 17 is a growth factor for pancreatic, stomach and colorectal cancers, and a potent stimulator of gastric acid secretion.The anti-gastrin immunogen, G17DT, consists of a large carrier protein, called Diptheria Toxoid (DT). A synthetic peptide, which is similar to a portion of the gastrin 17 hormone (GT), is attached to the carrier protein. These are then contained in a liquid suspension vehicle. When administered to patients, G17DT induces an immune response producing antibodies, which cross-react and neutralise the target hormone thus preventing its interaction with disease-causing or -participating cells. Aphton has entered into an agreement with Aventis Pasteur for the marketing of G17DT in all human cancer indications in North America and Europe. Under the terms of the agreement, Aphton is responsible for product development, clinical trials and regulatory agency approvals. The agreement was originally with Pasteur Mérieux Connaught, a subsidiary of Rhône-Poulenc. However, in December 1999, Rhône-Poulenc merged with Hoechst to form Aventis. As a result of the merger, Pasteur Mérieux Connaught underwent a name change to Aventis Pasteur. In July 2002, Aphton announced that it would negotiate with companies wanting to licence the vaccine in territories other than North America and Europe. In February 2003, Aphton announced it had received fast track designation for G17DT in combination with cisplatin and fluorouracil for use in stage IV gastric cancer to improve overall survival. In July 2002, the US FDA granted G17DT orphan drug status for the treatment of gastric cancer, an indication that was broader than the indication Aphton originally sought. The vaccine was also granted orphan drug status in Australia for gastric cancer in December 2002. In July 2002, Aphton announced that the US FDA had granted G17DT orphan drug status for the treatment of adenocarcinoma of the pancreas. In September 2002, the US FDA also granted G17DT, used in combination with gemcitabine, fast track status for the treatment of pancreatic cancer patients. In addition, the vaccine was also granted orphan drug status in Australia for pancreatic cancer in December 2002. In March 2003, Aphton announced that the Committee for Orphan Medicinal Products had recommended to the European Commission that G17DT be granted orph

Topics: Animals; Cancer Vaccines; Clinical Trials as Topic; Colorectal Neoplasms; Gastrins; Humans; Orphan Drug Production; Pancreatic Neoplasms; Peptic Ulcer; Rats; Stomach Neoplasms; Vaccines

Most patients with peptic ulcer disease are currently treated with proton pump inhibitors or histamine H(2) receptor antagonists. The long-term use of these compounds has been associated with two potential problems. Firstly, proton pump inhibitors may induce enterochromaffin-like (ECL) cell hyperplasia. Secondly, ulcers may relapse despite maintenance therapy with histamine H(2) antagonists. This has been the rationale for the development of new antisecretory agents, including antagonists against gastrin and gastrin releasing peptide (GRP), as well as ligands to histamine H(3) receptors. Several potent, high affinity cholecystokinin (CCK)-2 receptor antagonists have recently been identified such as L-365260, YM-022, RP-73870, S-0509, spiroglumide and itriglumide (CR-2945). Current data suggest that they all have antisecretory and anti-ulcer effects. In addition to reducing acid production, CCK-2 receptor antagonists may possibly also accelerate gastric emptying, a combination of functions which could potentially be beneficial in patients with functional dyspepsia. Receptors for bombesin and its mammalian counterpart GRP have been localised in the brain, spinal cord and enteric nerve fibres of the gut as well as on secretory cells and smooth muscle cells of the intestinal tract. Current data clearly indicate that endogenous GRP is involved in the regulation of basal and postprandial acid secretion. However, at this stage it is not clear whether GRP agonists or GRP antagonists can be developed into useful drugs. The peptide has a wide range of biological effects and it is likely that analogues of GRP or antagonists of the peptide affect not only gastric acid secretion but also induce considerable side effects. Histamine plays a central role in the stimulation of acid secretion. After their detection in the brain, H(3) receptors have been identified in a variety of tissues including perivascular nerve terminals, enteric ganglia of the ileum and lung, and ECL cells. Despite many studies, the role of H(3) receptors in the regulation of gastric acid secretion is still unclear. Controversial data have been presented, and study results largely depend on the species and experimental models. It seems unlikely that proton pump inhibitors or H(2) receptor antagonists will be replaced in the near future by new antisecretory agents. The current shortcomings of the new compounds include mainly their reduced clinical effectiveness and pharmacological limitations. However

Topics: Animals; Gastric Acid; Gastrin-Releasing Peptide; Gastrins; Histamine Antagonists; Humans; Ligands; Peptic Ulcer; Receptor, Cholecystokinin B; Receptors, Bombesin; Receptors, Histamine H3

On the basis of the levels of serum pepsinogen I (S-PGI) and gastrin-17 (S-G-17) as well as Helicobacter pylori - antibodies assayed from a blood sample it is possible to establish with high sensitivity and specificity whether the patient has gastritis, whether the gastritis is atrophic or not and in which part of the stomach the atrophic changes are located. The test enables the identification of patients whose risk of gastric cancer, of the consequences of vitamin B12 deficiency (e.g. elevated levels of homocysteine) or of peptic ulcer is considerably increased and who can then undergo gastroscopy. It also facilitates the diagnosis of non-atrophic Helicobacter gastritis enabling treatment before endoscopy.

Topics: Finland; Gastrins; Gastritis, Atrophic; Helicobacter Infections; Humans; Pepsinogen A; Peptic Ulcer; Stomach Neoplasms; Vitamin B 12 Deficiency

Gastrin stimulates gastric acid secretion through direct activation of CCK-B/gastrin receptors on parietal cells and indirectly through release of histamine from ECL cells. Cholecystokinin (CCK) is structurally closely related to gastrin and shares high affinity for CCK-B/gastrin receptors. In contrast to gastrin, CCK also recognizes CCK-A receptors. While CCK appears to be a negative regulator of gastric acid secretion and postprandial release of gastrin in the normal human gastrointestinal tract, its impact on the pathogenesis of acid hypersecretion in Helicobacter pylori-infected individuals remains uncertain. This article will review the endocrine and paracrine regulatory pathways which are activated by CCK/gastrin peptides and which appear relevant in the pathogenesis of peptic ulcer disease in man.

Topics: Gastric Acid; Gastric Mucosa; Gastrins; Humans; Molecular Biology; Peptic Ulcer; Receptors, Cholecystokinin

Topics: Acetylcholine; Animals; Calcitonin Gene-Related Peptide; Epinephrine; Galanin; Gastric Acid; Gastrins; Ghrelin; Humans; Interleukin-1; Neuropeptides; Peptic Ulcer; Peptide Hormones; Peptides; Pituitary Adenylate Cyclase-Activating Polypeptide; Prostaglandins E; Somatostatin

The decline in duodenal ulcer disease and the established relation of peptic ulcer to Helicobacter pylori have virtually abolished the need for elective ulcer surgery. However, a substantial proportion of the population around retirement age has previously been subjected to partial gastric resection due to peptic ulcer, and the long-term outcome of these patients is of continuing relevance. Patients subjected to elective surgery could represent a selected group of healthy subjects with a lower overall morbidity, but reports indicate that patients operated on for peptic ulcer have more advanced disease associated with excess smoking and a different pattern of social behavior. The surgical procedure induces enterogastric reflux, leading to profound changes in the remnant mucosa and the formation of carcinogens in the gastric juice. In addition, metabolic abnormalities are common, especially fat malabsorption. Evaluation of the impact of these factors on morbidity and mortality is difficult. Increased mortality in gastrointestinal tumors (especially gastric stump carcinoma), respiratory diseases and other smoking-related malignancies, and suicide are found in the long-term follow-up after partial gastric resection due to peptic ulcer. However, these hazards to life are offset by a decreased mortality in cardiovascular disease. Preventive measures against suicide and especially tobacco smoking are recommended to improve th outcome for this cohort.

Topics: Bile Reflux; Cardiovascular Diseases; Female; Gastrectomy; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Nutrition Disorders; Peptic Ulcer; Prognosis; Risk Factors; Sex Factors; Smoking; Stomach Neoplasms; Suicide; Time Factors

Helicobacter pylori (H. pylori) infection leads to profound changes in gastric physiology. Several clinical and animal studies have been performed to clarify the influence of H. pylori on gastric acid secretion. Published data, however, are not consistent throughout. Infection of the gastric antrum, which can be observed mainly in duodenal ulcer patients, increases gastrin release and consecutively acid output. The net effect of corpus and antrum gastritis, such as in patients with gastric cancer, is to decrease acid secretion. Chronic H. pylori infection may finally promote gastric atrophy with irreversibly diminished acid secretion but in earlier stages of this infection eradication of H. pylori normalizes gastric secretory activity.

Topics: Animals; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Peptic Ulcer; Somatostatin

Helicobacter pylori is the cause of chronic type B gastritis and occurs in almost all patients with duodenal ulcers. Infection with H. pylori is characterized by an increased production of several inflammatory cytokines. Increasing evidence suggests a central role of these cytokines in the pathogenesis of H. pylori-associated gastritis and peptic ulcer disease. Cytokines may be crucial in the recruitment and activation of inflammatory cells and in stimulation of gastrin release. In addition to their proinflammatory properties, cytokines may also inhibit the ulcer occurrence by stimulation of prostaglandins and somatostatin release and by direct impairment of acid secretion. The balance of these factors may determine the clinical outcome of H. pylori infection.

Topics: Animals; Cytokines; Duodenal Ulcer; Gastrins; Gastritis; Genes, MHC Class II; Helicobacter Infections; Helicobacter pylori; Humans; Inflammation; Intestinal Mucosa; Peptic Ulcer; Somatostatin

The study of gastrin continues to serve as an excellent model for gastrointestinal regulatory processes. This review highlights some recent advances in the field by outlining gastrin biosynthesis, summarizing current understanding of gastrin receptors, describing the regulation of gastrin release, and discussing the clinical implications of gastrin in the pathogenesis of peptic ulcer disease. Emphasis is on three emerging areas of gastrin research: the novel finding that one of gastrin's posttranslational processing intermediates has biological activity distinct from that of the mature peptide; elucidation of gastrin's signal transduction mechanisms that mediate the trophic effects of the peptide; and the role of gastrin in peptic ulcer disease pathogenesis secondary to Helicobacter pylori infection.

Topics: Animals; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Protein Processing, Post-Translational; Receptors, Cholecystokinin; Stomach

Concerns have been raised regarding the safety of proton pump inhibitors in the long-term management of acid-related peptic disease, especially with regard to the physiological effects of prolonged hypochlorhydria. Of special consideration is the potential for development of enterochromaffin-like cell hyperplasia and gastric carcinoids, colorectal adenocarcinoma and polyps, and bacterial overgrowth as a result of achlorhydria. However, the magnitude of hypergastrinemia associated with the administration of proton pump inhibitors is comparable to that observed after vagotomy and is 3- to 6-fold lower than that observed with pernicious anemia. Only minimal morphological changes in gastric endocrine cells have been observed after the long-term daily administration of proton pump inhibitors, and these changes appear to be self-limiting, nondysplastic, and nonneoplastic. All current evidence suggests that the hypergastrinemia observed during proton pump inhibitor therapy has little clinical significance. However, longer-term results are necessary so that one can appreciate the full implications of acid suppression by proton pump inhibitors.

Topics: Antacids; Anti-Ulcer Agents; Drug Interactions; Gastrins; Histamine H2 Antagonists; Humans; Peptic Ulcer; Proton Pump Inhibitors; Safety; Time Factors

Gastric mucosa is exposed to various aggressive factors such as stress, ulcerogenic drugs including acetyl-salicylic acid(ASA)-like agents, ethanol, bacteria, particularly Helicobacter pylori (Hp), and various endogenous irritants such as acid-pepsin secretion and bile salts. The maintenance of the mucosal barrier depends upon the activation of the pre-epithelial (mucus-alkali secretion), epithelial (surface-active phospholipids and rapid mucosal restitution) and post-epithelial (mucosal microcirculation, sensory nerves and mast cells) components of mucosal defense. Ebrotidine (N-[(E)-[[2-[[[2-[(diaminomethylene)amino]- 4-thiazolyl]methyl]thio]ethyl]amino]methylene]-4-bromo-benzenesulfonamid e, CAS 100981-43-9, FI-3542) is the first of a new generation of H2-receptor antagonists with both antisecretory and cytoprotective activities. Its inhibitory action is similar to that of ranitidine and approximately tenfold greater than cimetidine, and is accompanied by a small and transient increase in plasma gastrin levels. In contrast to ranitidine and other H2-receptor antagonists, ebrotidine exerts a unique cytoprotection against injury by various ulcerogens such as ethanol, ammonia, lipopolysaccharides (LPS), stress and ASA or acidified taurocholate. The mechanism of this protection by ebrotidine is not clear, but it has been shown to stimulate mucus secretion, to increase the quality of adherent mucus gel and to increase gastric mucosal blood flow (GBF), possibly due to enhanced mucosal formation of prostaglandin E2 (PGE2) and nitric oxide (NO). The cytoprotective effects of ebrotidine were observed in rats and confirmed also in humans with gastric lesions induced by ethanol or ASA. Ebrotidine also exerts anti-Helicobacter pylori (Hp) effects by interfering with surface receptors of epithelial cells and inhibiting urease, protease and lipase activity, and by counteracting the noxious effects of Hp-related substances such as ammonia and lipopoly-saccharides (LPS).

Topics: Adult; Animals; Benzenesulfonates; Gastric Acid; Gastric Mucosa; Gastrins; Histamine H2 Antagonists; Humans; Male; Peptic Ulcer; Ranitidine; Rats; Rats, Wistar; Thiazoles

The dictum "no acid-no ulcer" had, in the past, summarized the thinking concerning the pathogenesis of peptic ulcer disease. It is now recognized that infection with Helicobacter pylori is the major causal factor leading to both duodenal and gastric ulceration. Infection is associated with many of the acid secretory abnormalities that have traditionally characterized peptic ulcer disease; indeed, acid secretory physiology returns to normal following bacterial eradication. Since not all individuals infected with H. pylori develop ulcers, host susceptibility, bacterial virulence, and/or specific environmental factors must determine the response to infection and the ultimate clinical outcome. The relative importance of these factors and their complex interactions remain to be determined. H. pylori infection produces tissue damage indirectly because the organism does not directly invade gastroduodenal tissue. A variety of bacterial enzymes, toxins, and inflammatory mediators produced in response to bacterial colonization challenge the integrity of host mucosal defenses. In a susceptible host, breached defenses render epithelium more vulnerable to acid injury and ulcer development. Eradication of H. pylori leads to rapid ulcer healing and reversal of tissue injury, thereby obviating ulcer recurrence.

Topics: Duodenal Ulcer; Gastric Acid; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Peptic Ulcer; Stomach Ulcer

Topics: Gastric Acid; Gastrins; Helicobacter pylori; Humans; Pepsin A; Peptic Ulcer

Gastrin releasing peptide (GRP) has proved to be a particularly valuable tool in detecting disturbances of gastric secretory function associated with duodenal ulcer disease and Helicobacter pylori infection, and it has furthered understanding of the pathophysiology of these conditions. Its attractiveness lies in the fact that it simultaneously activates many physiological control processes, both stimulatory and inhibitory. This facilitates the detection of a defect in any of the many controls involved in regulating biological function. Other gastrointestinal functions such as gall-bladder contraction, pancreatic secretion and gastrooesophageal motility are also subject to complex regulatory controls, and GRP may also be of value in investigating disturbances of these processes.

Topics: Duodenal Ulcer; Gastric Acid; Gastrins; Helicobacter pylori; Humans; Peptic Ulcer; Peptides; Receptors, Bombesin

Etiologic role for HP appears to be best established in histologically proven gastritis. The major factors mediating gastritis induced by the colonization of the "gastric type" mucosa with HP are probably cytotoxins, cytokines and free radicals activated by this organisms. The deficiency of negative feedback in somatostatin-gastrin link in antral gastritis may result in an excessive gastrin release and increased gastric acid secretion with increased duodenal acid load under basal state and after meal. Recent NIH consensus 1994 proposes that: (1) ulcer patients with HP require treatment with antimicrobial agents whether on first presentation or on recurrence; (2) the value of treatment of HP infection in non-ulcer dyspepsia remains to be determined and (3) the asymptomatic subjects with HP infection do not require treatment with antimicrobial agents.

Topics: Bacteriological Techniques; Bicarbonates; Duodenal Ulcer; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Peptic Ulcer

Topics: Analgesics; Blood Group Antigens; Diet; Duodenitis; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Metaplasia; Peptic Ulcer; Risk Factors; Smoking; Stress, Physiological; Twin Studies as Topic

Topics: Achlorhydria; Antacids; Anti-Ulcer Agents; Gastric Acid; Gastrins; Gastroesophageal Reflux; Humans; Peptic Ulcer; Time Factors

Drug-induced achlorhydria in experimental animals results in excessive hypergastrinaemia, ECL-cell hyperplasia and ECL-cell carcinoidosis. However, these events have not been observed in long-term studies in patients receiving proton pump inhibitors. Serum gastrin levels increase only modestly during acute and long-term treatment. It is concluded that monitoring of serum gastrin levels and of fundic ECL cells is of no clinical relevance even during long-term therapy with proton pump inhibitors. The clinically available proton pump inhibitors such as pantoprazole, omeprazole and lansoprazole are well tolerated, with a low incidence of side-effects. Minor and serious side-effects classified as possibly related to proton pump therapy have been described in up to 2.5% of patients. This is the same order of magnitude as that found in patients treated with H2-receptor blockers and in placebo-treated controls. In most cases, therefore, the observed side-effects are unrelated to the intake of proton pump inhibitors. Minor adverse events include headache, diarrhoea, dizziness, pruritus and rash. Proton pump inhibitors are metabolized mainly in the liver via the cytochrome P450 system and interactions with drugs metabolized by the same system are possible. Evidence is becoming available which suggests that pantoprazole may have less potential to interact with the cytochrome P450 system than the other proton pump inhibitors. In the case of diazepam metabolism, pantoprazole had the least effect on prolongation of the diazepam effect. This may well be an advantage in the clinical use of the drug.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Animals; Benzimidazoles; Cytochrome P-450 Enzyme System; Disease Models, Animal; Drug Interactions; Enterochromaffin Cells; Gastrins; Humans; Lansoprazole; Omeprazole; Pantoprazole; Peptic Ulcer; Proton Pump Inhibitors; Sulfoxides

In the high altitude environment the oxygen and air density are decreased, the temperature and humidity are low, there es an increase in radioactivity. These environmental factors influence on the human body; it has been known for many years that people born and living at high altitude have different morphological and physiological characteristic than those at low altitude. The digestive mechanism for adaptation or acclimation to high altitude has interested physiologist and clinicians for many years. The objective of this article is to present a brief overview of the digestive physiology and pathology in the high altitude.

Topics: Altitude; Bolivia; Cholelithiasis; Colonic Neoplasms; Diverticulum, Colon; Dyspepsia; Endopeptidases; Gallbladder Neoplasms; Gastric Mucosa; Gastrins; Gastrointestinal Diseases; Gastrointestinal Hemorrhage; Gastrointestinal Transit; Humans; Intestinal Obstruction; Intestines; Peptic Ulcer; Peru

Recent studies have been reviewed to establish the possible importance of the interaction between Helicobacter pylori infection and gastric acid secretion. H. pylori infection results in increased gastrin release, but this does not lead to gastric acid hypersecretion and gastrin normalizes after eradication of the infection. An optimal, well-tolerated treatment strategy against H. pylori infection has not yet been clearly defined. One potentially useful approach may be to improve the antibacterial efficacy of antibiotics by effectively regulating gastric acidity. H2-receptor antagonists have no effect against H. pylori infection, while omeprazole (an acid pump inhibitor) appears to have a bacteriostatic action. Combination therapy with omeprazole and amoxycillin has been found to eradicate H. pylori in 50-80% of patients with duodenal ulcer, leading to a significant reduction in ulcer recurrence.

Topics: Amoxicillin; Clinical Trials as Topic; Drug Synergism; Drug Therapy, Combination; Gastric Acid; Gastric Acidity Determination; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Omeprazole; Peptic Ulcer; Recurrence; Stomach Diseases

Topics: Animals; Gastric Acid; Gastrins; Humans; Peptic Ulcer

Gastrin represents a direct pathogenic factor only in rare subgroups of ulcer patients, such as in the Zollinger-Ellison syndrome, the antral G-cell hyperplasia syndrome, and in patients in whom the gastric antrum was erroneously retained following partial gastrectomy. Gastrin may play a contributory role in the pathogenesis of uncomplicated peptic ulcer disease, as an exaggerated, but reversible gastrin release appears to be associated with Helicobacter pylori colonization. The known trophic effects of gastrin could account for the overall increase in the parietal cell mass of patients suffering from duodenal ulcer disease. Circumstantial evidence suggests that the abnormal gastrin release could also explain the upregulation of the parietal cell to the acid stimulatory effect and the consequent increase in gastrin sensitivity in patients suffering from duodenal ulcer disease. Conversely, the trophic effects of gastrin have also been linked to ulcer healing, especially since potent acid inhibitors induce a substantial hypergastrinemia. The evidence for such an association, however, is only circumstantial and potent and selective gastrin receptor antagonists are necessary to fully clarify the role gastrin exerts in ulcer healing.

Topics: Animals; Epithelium; Gastric Mucosa; Gastrins; Humans; Pentagastrin; Peptic Ulcer; Rats; Wound Healing

Proliferation and growth of gastroduodenal mucosal cells represent important elements of mucosal defense and any alterations in the balance between cell proliferation and cell loss may lead to trophic changes in mucosa. Acute mucosal lesions induced by local irritants such as bile salts, ethanol, aspirin, or stress are accompanied by widespread damage of surface epithelium followed by almost immediate repair due to mucosal cell restitution, which is unrelated to cell proliferation but does depend on the intrinsic property of mucosal cells to cover superficial defects. Cytoprotection involves the protection of the regeneration zone and the maintenance of blood flow to the mucosa. Various factors that exhibit mucosal growth-promoting action include EGF, gastrin, growth hormone, and GH-releasing factor. These factors protect the mucosa against acute injury but the mechanism of this effect is not clear. These trophic agents, especially EGF, accelerate the healing of chronic gastroduodenal ulceration and may contribute to the healing effects of sucralfate or De-Nol. These effects of trophic substances are related to their stimulation of cell proliferation and DNA, RNA, and protein synthesis and can be reversed by the suppression of mucosal growth. Prostaglandins, especially their stable methylated analogs, display trophic effects on the gastric mucosa but neither gastroprotective nor ulcer healing actions of PG can be attributed to their trophic effect. With increasing attention being paid to mucosal growth and repair as components of mucosal defense, the emphasis of drug therapy of acute or chronic gastroduodenal lesions is likely to move toward strengthening mucosal defense rather than the inhibition of aggressive factors.

Topics: Animals; Duodenum; Epidermal Growth Factor; Gastrins; Growth Substances; Humans; Peptic Ulcer; Prostaglandins; Secretin; Somatostatin; Stomach

Acid secretion is regulated by hormonal factors acting peripherally and centrally, as well as neural factors. Gastrin and histamine are the two most important peripheral hormonal stimulants, while the vagus is the predominant nerve affecting acid secretion. Meal related acid secretion occurs in three phases: cephalic, gastric and intestinal. Acid secretion is stimulated in the first two phases while it is inhibited in the intestinal phase. Proteins are potent acid stimulants but carbohydrates and fats are inhibitors. Tea, coffee, milk and alcohol are acid stimulants; on the other hand the damaging influence of spices on the stomach may not be related to increased acid secretion. Psychological stress has a variable effect. The effect of Helicobacter pylori infection on acid secretion is being elucidated. Many drugs modifying acid secretion are available and are useful in the treatment of acid peptic disease.

Topics: Digestion; Gastric Acid; Gastrins; Histamine; Humans; Peptic Ulcer; Somatostatin

Acid and pepsin are the major aggressive factors believed to play a role in the pathogenesis of peptic ulcer disease. On the average, patients with duodenal ulcer disease have higher than normal basal, nocturnal, and pentagastrin-stimulated acid secretion. Food-stimulated acid secretion, however, is normal in duodenal ulcer patients. The reason for higher basal and nocturnal acid secretion is not known but may be secondary to higher than normal basal serum gastrin concentrations in duodenal ulcer patients. Average serum pepsinogen levels also are higher than normal in patients with duodenal ulcer disease, suggesting that luminal pepsin concentrations also are higher. Patients with gastric ulcers have either normal or lower than normal acid secretion. This suggests that factors other than acid and pepsin may play a role in causing gastric ulcers. Reflux of bile and pancreatic juice into the stomach of patients with gastric ulcers has been suggested as one of the aggressive factors playing a role in the development of gastric ulcers.

Topics: Duodenogastric Reflux; Female; Food; Gastric Acid; Gastrins; Humans; Male; Pepsin A; Pepsinogens; Peptic Ulcer

Topics: Gastric Acid; Gastrins; Histamine H2 Antagonists; Humans; Infections; Malabsorption Syndromes; Peptic Ulcer; Risk Factors

Topics: Duodenal Ulcer; Gastric Mucosa; Gastrins; Humans; Parietal Cells, Gastric; Peptic Ulcer; Vagus Nerve

Single doses of omeprazole inhibit pentagastrin-stimulated gastric acid secretion and almost complete inhibition can be achieved for 4-6 hours with a single dose of 80 mg. Acid secretion then slowly returns and reaches normal levels after 3-4 days. Omeprazole also dose-dependently inhibits basal acid secretion as well as acid secretion stimulated with histamine, peptone and modified sham feeding, with similar efficiency. During repeated once-daily dosing with an enteric-coated granule capsule formulation, inhibition of acid secretion increased initially, and stabilized within about 4 days. Dose-response studies in patients with duodenal ulcers and healthy subjects have shown that 20-40 mg/day results in a peak reduction (80-100%) of pentagastrin-stimulated acid secretion 6 hours after dose. Studies of 24-hour intragastric acidity in duodenal ulcer patients have shown that 4 weeks of treatment with omeprazole, 20 mg once daily, resulted in a reduction of median intragastric acidity by 97%, which was superior to the 57% median reduction achieved with ranitidine, 150 mg b.d., for 4 weeks in the same patients. During omeprazole treatment, fasting plasma gastrin increased in relation to the degree of inhibition of acid secretion. After discontinuation of treatment, plasma gastrin normalized. Treatment with omeprazole, 20 mg, increased 24-hour plasma gastrin to the same extent as after highly selective vagotomy. Long-term treatment with omeprazole, 20-40 mg, for up to 2 years has not been associated with any progressive rise in fasting plasma gastrin.

Topics: Dose-Response Relationship, Drug; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Omeprazole; Parietal Cells, Gastric; Peptic Ulcer

Although the pathogenetic role of gastrin in gastric acid hypersecretion and peptic ulcer is well established in a number of uncommon disorders, such as Zollinger-Ellison syndrome, antral G-cell hyperfunction, and retained, excluded antrum after subtotal gastrectomy, the significance of hormonal abnormalities in normogastrinaemic peptic ulcer is less obvious. Most studies have pointed to an impaired feedback mechanism between gastric acid and antral gastrin secretion in duodenal ulcer disease, possibly due to antral somatostatin deficiency. Furthermore, antisecretory drugs may induce abnormalities of gastrointestinal hormones. Potent antisecretory drugs, such as omeprazole, increase serum and antral gastrin and reduce antral somatostatin, whereas certain prostaglandin E2 analogues inhibit serum gastrin secretion after feeding.

Topics: Animals; Anti-Ulcer Agents; Feedback; Gastric Acid; Gastrins; Humans; Peptic Ulcer; Somatostatin

Gastrin, a polypeptide hormone secreted by G (gastrin)-cells in the antroduodenal mucosa, is not only a potent stimulant of gastric acid secretion but also exerts trophic actions on the parietal, chief and enterochromaffin-like cells in the oxyntic mucosa. Gastrin plays a crucial role in the pathogenesis of hypergastrinaemic peptic ulcer disease, i.e. in the Zollinger-Ellison syndrome, antral G-cell hyperfunction and retained excluded antrum after subtotal gastrectomy. In patients with normogastrinaemic duodenal ulcer disease the feedback mechanism between gastric acid and gastrin secretion is impaired, while in gastric ulcer patients gastrin secretion is appropriately regulated by gastric acid. Antisecretory drugs may exert varying effects on gastrin secretion. Potent antisecretory drugs, such as omeprazole, increase serum and antral gastrin concentrations, whereas histamine H2-receptor antagonists, such as cimetidine, ranitidine, famotidine and roxatidine, have little influence on gastrin. Interestingly, antisecretory doses of prostaglandin E2-analogues, such as enprostil and arbaprostil [15(R)-15-methylprostaglandin E2], inhibit gastrin secretion, while gastrin is not influenced by prostaglandin E1-analogues, e.g. misoprostol. Somatostatin and the somatostatin-analogue SMS 201-995 reduce serum gastrin levels and gastric acid secretion.

Topics: Anti-Ulcer Agents; Gastrins; Humans; Peptic Ulcer

Recent advances in understanding the physiology and pathophysiology of the gastrointestinal hormone, gastrin, are reviewed. Details of gastrin biosynthesis, secretion, and cellular actions may have broad implications for other peptide hormones. Potentially useful antigastrin drugs are described. Areas of future development are suggested.

Topics: DNA Replication; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Receptors, Gastrointestinal Hormone; Stomach Neoplasms; Vagotomy; Zollinger-Ellison Syndrome

Topics: Antacids; Anti-Ulcer Agents; Carbenoxolone; Gastrins; Histamine Antagonists; Histamine H2 Antagonists; Humans; Mineral Waters; Organometallic Compounds; Parasympatholytics; Peptic Ulcer; Sucralfate

This investigation examined the effect of rioprostil, a primary alcohol prostaglandin E1 analog, on betazole-stimulated gastric acid secretion and on basal and food-stimulated (postprandial) serum gastrin levels in gastric fistula dogs. Rioprostil inhibited betazole-stimulated gastric acid secretion with an ED50 of 16 (10-24) micrograms/kg, intragastrically. A near-maximal gastric antisecretory dose (100 micrograms/kg, intragastrically) had no effect on basal serum gastrin levels but significantly attenuated the rapid rise in serum gastrin which follows feeding, a result different from that reported for other prostaglandin E1 analogs. A nonantisecretory dose of rioprostil (1.0 micrograms/kg, intragastrically) also attenuated the rise in postprandial serum gastrin. An antigastrin effect using a nonantisecretory dose of an antiulcer agent has not been reported previously and may indicate that rioprostil has a direct inhibitory effect on secretion of gastrin. The ability of rioprostil to inhibit gastric acid secretion and decrease postprandial peak serum gastrin levels, coupled with previously established cytoprotective efficacy, makes it an attractive clinical candidate for the treatment and prevention of peptic ulcer disease.

Topics: Animals; Anti-Ulcer Agents; Depression, Chemical; Dogs; Female; Gastric Acid; Gastric Fistula; Gastrins; Gastrointestinal Contents; Peptic Ulcer; Prostaglandins E; Radioimmunoassay; Rioprostil

Gastrin is the most important peptide in the regulation of gastric acid secretion. This communication reviews important new developments in our knowledge of its synthesis, action, and pathophysiology. The gene for human gastrin has been isolated, and it encodes a pre-pro-gastrin which is a 101-aminoacid peptide containing within it the structure of big gastrin (G34) with a C-terminal glycine extension. Post-translational processing by alpha-amidation of the glycine-extended progastrin results in generation of the active forms of the peptide (G34, G17). When gastrin binds to its receptor on the parietal cell, phosphatidylinositol biphosphate (IP2) in the plasma membrane is converted to inositol 1,4,5-triphosphate (IP3), which acts as the secondary intracellular messenger to increase intracellular calcium and initiate the process that eventually leads to acid secretion. Although an abnormality in gastrin release or action is not thought to be crucially important in the genesis of duodenal ulcer, these patients nevertheless demonstrate increased postprandial gastrin release, and a greater sensitivity of their parietal cells to gastrin. Hypergastrinemia is the cause of peptic ulceration in the Zollinger-Ellison syndrome, in primary gastrin cell hyperplasia or hyperfunction, and in the retained antrum syndrome. Ulcerogenic hypergastrinemia must be distinguished from hypergastrinemia that is secondary to hypoacidity or anacidity, as is seen in atrophic gastritis or postvagotomy.

Topics: Female; Gastrectomy; Gastric Acid; Gastrins; Humans; Male; Parietal Cells, Gastric; Peptic Ulcer; Pyloric Antrum; Zollinger-Ellison Syndrome

Greatly improved understanding of the cellular basis for gastric acid secretion and gastroduodenal mucosal defense has led to a dramatic improvement in the pharmacologic treatment of peptic ulcer disease. The advances produced by cimetidine and ranitidine are being continued by a new generation of histamine receptor antagonists, as well as by other anti-ulcer agents. These new drugs, when used appropriately, will greatly expand the surgeon's ability to treat patients with peptic ulcer disease. A knowledge of the pathophysiologic characteristics of peptic ulceration and of the inherent limitations of each agent will become increasingly important for surgeons who treat these patients.

Topics: Acetylcholine; Benzimidazoles; Chemical Phenomena; Chemistry; Cimetidine; Disease Susceptibility; Dose-Response Relationship, Drug; Duodenal Ulcer; Gastric Acid; Gastric Mucosa; Gastrins; Histamine; Histamine H2 Antagonists; Humans; Imidazoles; Intestinal Mucosa; Peptic Ulcer; Ranitidine; Receptors, Muscarinic; Stimulation, Chemical; Stomach Ulcer

Topics: Gastric Acid; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Pyloric Antrum; Vagotomy

Topics: Anemia, Pernicious; Gastric Acid; Gastric Emptying; Gastrins; Gastritis, Atrophic; Genetic Markers; Humans; Pepsinogens; Peptic Ulcer

Topics: Disease Susceptibility; Dysgammaglobulinemia; Gastric Mucosa; Gastrins; Humans; IgA Deficiency; Pepsinogens; Peptic Ulcer

Topics: Acute Kidney Injury; Bile; Digestive System Diseases; Gastrins; Gastritis; Humans; Kidney; Kidney Failure, Chronic; Peptic Ulcer

Pirenzepine is a 'selective' antimuscarinic agent which, unlike classic anticholinergic agents, inhibits gastric acid secretion at lower doses than are required to affect gastrointestinal motility, salivary, central nervous system, cardiovascular, ocular and urinary functions. On a weight basis, pirenzepine has one-tenth to one-eighth the potency of atropine in inhibiting stimulated gastric acid secretion in humans. Extensive controlled trials utilising endoscopy in outpatients with duodenal ulcers indicate that patient response to pirenzepine is dose related. Doses of 100 to 150 mg/day are superior to placebo in promoting duodenal ulcer healing and in diminishing day and night pain and supplementary antacid consumption. At such doses, the efficacy of pirenzepine appears to be superior to that of gefarnate 300 mg/day and generally not significantly different from that of cimetidine 1 g/day in treating duodenal ulcers. A beneficial effect of pirenzepine in the prevention of duodenal ulcer recurrence was apparent in preliminary studies in small numbers of patients, but its efficacy in this regard needs further confirmation and the optimum dosage determined. Less extensive data on the treatment of benign gastric ulcers suggest that pirenzepine 100 to 150 mg/day is superior to placebo and gefarnate 300 mg/day and does not differ significantly from cimetidine 1 g/day promoting gastric ulcer healing. Pirenzepine is well tolerated by most patients, with a low incidence of typical antimuscarinic effects on the gastrointestinal tract, genitourinary system or heart being reported in clinical studies. However, dry mouth and blurred vision are the more common side effects with clinically effective doses. Thus, pirenzepine appears to have relatively selective antimuscarinic activity, although controlled studies comparing pirenzepine and conventional antimuscarinics in patients with peptic ulcer disease have not been reported.

Topics: Benzodiazepinones; Dialysis; Dyspepsia; Gastric Acid; Gastrins; Gastrointestinal Hormones; Humans; Intestinal Absorption; Intestinal Mucosa; Kinetics; Nitrates; Pancreas; Parasympatholytics; Pepsin A; Peptic Ulcer; Pirenzepine; Receptors, Muscarinic; Recurrence; Tissue Distribution; Zollinger-Ellison Syndrome

Topics: Bombesin; Calcium; Eating; Gastric Emptying; Gastrins; Gastrointestinal Hormones; Histamine H2 Antagonists; Humans; Kidney Failure, Chronic; Peptic Ulcer; Pyloric Stenosis; Secretin; Vagotomy; Zollinger-Ellison Syndrome

Alpha-2 receptor activation mediates the inhibition of a number of gastrointestinal functions including gastric and intestinal secretions. Alpha-2 receptors are located in the brain and presynaptically on cholinergic nerve terminals; activation of either inhibits vagus nerve activity. Intestinal secretions are inhibited by postsynaptic alpha-2 receptors located on intestinal epithelial cells. Agents which selectively activate alpha-2 receptors in the gut may therefore be beneficial in treating gastric ulcers and diarrheal states. Two such agents which activate alpha-2 receptors in the gut are WHR-1370A [1-n-butoxy-3-(2,6-dimethylphenylcarbamoyl) guanidine hydrochloride] and lidamidine. WHR-1370A is a potent gastric antisecretory and antiulcer agent which inhibits the release of acetylcholine from the vagus nerve. WHR-1370A's activity is blocked by yohimbine. Lidamidine is a clinically effective antidiarrheal agent. Lidamidine's response is partially inhibited by yohimbine in animal diarrheal models. Alpha-2 agonists represent a new class of drugs which have a promising future in the treatment of gastrointestinal disorders.

Topics: Adrenergic alpha-Agonists; Animals; Antidiarrheals; Brain; Carbachol; Clonidine; Cysteamine; Deoxyglucose; Gastric Acid; Gastrins; Gastrointestinal Motility; Humans; Injections, Intraventricular; Norepinephrine; Peptic Ulcer; Phenylurea Compounds; Time Factors; Yohimbine

Topics: Animals; Anti-Ulcer Agents; Central Nervous System; Cimetidine; Drug Interactions; Endocrine System Diseases; Esophagogastric Junction; Gastrins; Histamine H2 Antagonists; Humans; Intraocular Pressure; Peptic Ulcer; Ranitidine; Rats; Receptors, Histamine H2

Topics: Animals; Dogs; Gastrins; Gastrointestinal Hormones; Humans; Intestine, Small; Kidney Failure, Chronic; Liver Cirrhosis; Malabsorption Syndromes; Peptic Ulcer; Postoperative Complications; Short Bowel Syndrome

Topics: Adenoma; Carcinoid Tumor; Endocrine System Diseases; Gastrins; Gastrointestinal Diseases; Glucagonoma; Histocytochemistry; Humans; Hyperinsulinism; Immunochemistry; Insulinoma; Islets of Langerhans; Pancreatic Diseases; Pancreatic Neoplasms; Peptic Ulcer; Somatostatinoma; Stomach; Vipoma

Topics: Diagnosis, Differential; Gastrins; Humans; Pancreatitis; Peptic Ulcer; Secretin

Sulfated gastrins resemble cholecystokinins (CCK) both structurally and functionally. They are less potent than CCK in stimulating gallbladder contraction and pancreatic enzyme secretion, but the plasma concentrations of sulfated gastrin are higher than those of CCK. Therefore, sulfated gastrins may contribute significantly to the endogenous CCK activity. The degree of sulfation of gastrin differs with the localization in the digestive tract. In the antrum and duodenum of normal subjects 45% of the gastrins are sulfated, as in serum. In contrast, the sulfation of gastrin is complete in the jejunum (human) and in the pancreas (rat and cat). Hence, the degree of sulfation of gastrin is similar to that of CCK in the jejunum. The degree of sulfation in antrum, duodenum and serum diminishes with hypergastrinemia, and is thus significantly lower in patients with gastric ulcer or pernicious anemia than in healthy subjects. In the Zollinger-Ellison syndrome, the degree of sulfation of gastrin varies greatly (20-90%) and the distribution between small and large gastrins is equally variable. However, sulfation and proteolytic processing follows a parallel course; complete processing to smaller components is accompanied by complete sulfation of the peptide and vice versa. During ontogenesis sulfated gastrins may be of special importance, since they are the only sulfated members of the gastrin/CCK family of peptides which occur in substantial quantities in the early fetus. Tyrosine-O-sulfation has now been recognized as a widespread modification, and sulfated tyrosyl residues in gastrin, CCK and leu-enkephalin are examples of a derivatization which can govern the biological activity of regulatory peptides.

Topics: Anemia, Pernicious; Animals; Duodenum; Gastrins; Humans; Jejunum; Pancreas; Peptic Ulcer; Pituitary Gland; Pyloric Antrum; Radioimmunoassay; Species Specificity; Sulfates; Tyrosine; Zollinger-Ellison Syndrome

Topics: Diabetes Mellitus; Gastrins; Humans; Pancreatic Hormones; Pancreatic Neoplasms; Peptic Ulcer; Somatostatin; Vasoactive Intestinal Peptide

Topics: Cyclic AMP; Female; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Male; Mucus; Neurotransmitter Agents; Pepsin A; Peptic Ulcer; Prostaglandins; Zollinger-Ellison Syndrome

Four patients with Zollinger-Ellison Syndrome (ZES) are presented to highlight the difficulties in the recognition, diagnosis and management of this rare disease. The presentation of ZES is usually indistinguishable from ordinary peptic ulcer disease and in those patients with symptoms not related to peptic ulcer, i.e., diarrhoea, as their main complaint, the diagnosis is often not even considered. A high index of suspicion is required, however, in patients with recurrent ulcers, multiple ulcers and in those with resistant or rapidly relapsing ulcers after conventional therapy. A presumptive diagnosis can be made by the demonstration of grossly elevated fasting serum gastrin levels combined with a secretin stimulation test in doubtful cases. The main problem is the location of the gastrin-secreting tumour which is usually pancreatic but often too small to be detected by currently available techniques. Histamine H2-receptor antagonists in high doses are effective in controlling the gastric acid hypersecretion which is chiefly responsible for the morbidity and mortality in ZES. They provide the treatment of choice in patients where the tumour cannot be located, though every attempt should be made to do this as surgery is the treatment of choice for this invariably malignant tumour. Total gastrectomy is now reserved for those patients in whom medical therapy has failed. The role of chemotherapy in metastatic disease has yet to be established.

Topics: Adult; Angiography; Diagnosis, Differential; Duodenoscopy; Female; Gastrectomy; Gastric Acid; Gastrins; Gastroscopy; Histamine H2 Antagonists; Humans; Male; Middle Aged; Peptic Ulcer; Tomography, X-Ray Computed; Ultrasonography; Zollinger-Ellison Syndrome

Topics: Calcium; Diagnosis, Differential; Duodenal Ulcer; False Negative Reactions; False Positive Reactions; Gastrectomy; Gastrins; Humans; Infusions, Parenteral; Injections, Intravenous; Jejunal Diseases; Peptic Ulcer; Secretin; Stomach Ulcer; Time Factors; Zollinger-Ellison Syndrome

Information concerning GEP hormones has progressively advanced since the initial discovery of a GEP hormone, secretin, in 1902. Studies in this area flourished with the advent of radioimmunoassay, and have provided an understanding of the secretion, regulation, metabolic actions, and role in certain diseases of major GEP hormones. Measurement of GEP hormones has achieved importance in clinical medicine and allowed understanding of the pathophysiology of several clinical disorders. The decade to come should witness additional advances in this rapidly expanding field.

Topics: Chemical Phenomena; Chemistry; Cholecystokinin; Diabetes Mellitus; Diarrhea; Endocrine System Diseases; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Hypoglycemia; Motilin; Neoplasms; Neurotensin; Pancreatic Polypeptide; Peptic Ulcer; Secretin; Skin Diseases; Somatostatin; Substance P; Vasoactive Intestinal Peptide

Antacids are neutralizing compounds which have been shown to hasten ulcer healing and to prevent bleeding from stress ulcerations. Owing to gastric alkalinization, gastrin will be released following antacid ingestion, a condition similar to that following the ingestion of a meal. Gastrin release and, more important, acid rebound also occur when the gastric mucosa comes into contact with calcium chloride. These findings indicate that acid rebound is independent of antral neutralization. Acid rebound and gastrin release will also be induced in duodenal ulcer patients by magnesium hydroxide. The magnitude of acid rebound represents one fourth to one third of the peak acid response to pentagastrin and is more marked following calcium than magnesium antacid intake. The mechanism of acid rebound may be in part due to gastrin release, but may also be due to the direct effect of calcium on the parietal cell. In the duodenum, calcium and magnesium evoke pancreatic enzyme secretion and gall bladder emptying. This effect of both cations is attributed to the release of cholecystokinin. Owing to their chemical composition, antacids stimulate the release of gastrointestinal hormones, cause acid secretion and stimulate pancreatic enzyme secretion and gall bladder concentration. So far, it has not been proven that these effects of antacids and of their chemical constituents will limit their therapeutic use.

Topics: Antacids; Bile; Calcium Carbonate; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Hormones; Humans; Intestinal Mucosa; Magnesium Hydroxide; Pancreas; Peptic Ulcer

Topics: Adolescent; Adult; Age Factors; Aged; Digestion; Fasting; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Middle Aged; Peptic Ulcer; Reference Values; Time Factors; Zollinger-Ellison Syndrome

Topics: Anemia, Pernicious; Depression, Chemical; Digestive System Physiological Phenomena; Gastric Acid; Gastrins; Hormones; Humans; Pancreatic Juice; Pepsin A; Peptic Ulcer; Somatostatin; Stomach Neoplasms

Topics: Antacids; Gastrins; Humans; Peptic Ulcer

Topics: Age Factors; Child; Child, Preschool; Gastric Juice; Gastrins; Humans; Infant; Infant, Newborn; Peptic Ulcer; Personality; United States

Gastrin release does play a part in the cephalic phase of acid secretion in man and is the major mechanism for the gastric phase of acid secretion. The vagal control of gastrin release is most likely mediated by cholinergic and possibly non-cholinergic excitatory fibres, as well as by cholinergic inhibitory fibres. Gastric luminal control of gastrin release is by local food and possibly distension stimulation, as well as by acid inhibition. Of the various causes of hypergastrinaemia, those associated with gastrinoma, G-cell hyperfunction and retained antrum have definite pathogenetic roles. Duodenal ulcer disease is a heterogeneous goup of disorders having different pathogenetic mechanisms. Parietal cell hyperplasia and G-cell dysfunctions, consisting of modest to florid G-cell hyperfunction and hyperplasia with secondary parietal cell hyperplasia, are but some facets of abnormalities that we have been able to identify.

Topics: Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hyperplasia; Peptic Ulcer; Pyloric Antrum; Vagus Nerve; Zollinger-Ellison Syndrome

Topics: Calcium; Diagnosis, Differential; False Positive Reactions; Food; Gastrectomy; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastroscopy; Glucagon; Humans; Magnesium Sulfate; Peptic Ulcer; Recurrence; Secretin; Zollinger-Ellison Syndrome

The importance of the gastrointestinal hormones to the clinician is considered under three headings: in disease states, diagnostic applications and therapeutic implications. Pearse's APUD (Amine Precursor Uptake and Decarboxylation) theory is referred to, and single and multiple endocrinopathies are discussed with particular referrence to diagnostic criteria and principles of management. The field of gastrointestinal endocrinology is rapidly developing and these peptides will assume an even greater importance to the clinician who must keep abreast with these developments.

Topics: Endoscopy; Esophagitis, Peptic; Gastrins; Gastrointestinal Hormones; Glucagon; Histamine; Humans; Multiple Endocrine Neoplasia; Peptic Ulcer; Secretin; Zollinger-Ellison Syndrome

Topics: APUD Cells; Cholecystokinin; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Motilin; Pancreatic Polypeptide; Peptic Ulcer; Secretin; Somatostatin; Vasoactive Intestinal Peptide

Topics: Anemia, Pernicious; Colon; Esophagus; Gastrectomy; Gastric Mucosa; Gastrins; Humans; Intestine, Small; Pancreas; Peptic Ulcer; Vagotomy

Topics: Antacids; Anti-Ulcer Agents; Bismuth; Carbenoxolone; Cimetidine; Clinical Trials as Topic; Costs and Cost Analysis; Gastric Juice; Gastrins; Humans; Parasympatholytics; Peptic Ulcer; Recurrence

Different types of vagotomy have been widely used in the treatment of peptic ulcer disease. A close relationship between the vagus nerve and the release or action of gastrointestinal hormones is necessary for the optimal activation of the gastrointestinal tract. The serum concentrations of the antral hormone gastrin are elevated after all types of vagotomy. The postvagotomy hypergastrinemia is due to the change in pH in the antral lumen or the gastric motility changes, both of which may lead to a proliferation of G cells. The reduction in pancreatic secretion after vagotomy is not due to changes in intestinal hormone release, but may be caused by the interruption of a postulated enteropancreatic reflex. Postprandial GIP release and serum insulin levels are not affected by vagotomy, but basal GIP levels are increased after vagotomy. Postprandial pancreatic polypeptide release is nearly abolished by vagotomy, but seems to normalize in the later postoperative course. These findings may be important for the interpretation of pathophysiologic changes after vagotomy.

Topics: Animals; Cholecystokinin; Dogs; Gastric Inhibitory Polypeptide; Gastrins; Gastrointestinal Hormones; Glucagon; Glucagon-Like Peptides; Humans; Insulin; Insulin Secretion; Pancreas; Pancreatic Polypeptide; Peptic Ulcer; Secretin; Somatostatin; Vagotomy

After reviewing the more recent acquisitions on the physiology and pathophysiology of gastrin, the authors concentrate on situations of hypergastrinemia, which they divide into a hyperhydrochloric and a hypohydrochloric variety. Among the former, which they subdivide into preoperative and postoperative, the authors discuss problems of differential diagnosis versus peptic ulcers in patients so afflicted. To that end they propose diagnostic policies comprising among other instrumental and laboratory tests the study of gastric secretion, blood gastrin levels in basal conditions and after stimulation by a protein meal, BBS, secretin, and calcium. From analysis of the results of such tests they were able to find a precise nosographic placement for postoperative hypergastrinemia, and from there they arrived at surgical programs aiming to correct postoperative peptic ulcers on the basis of their etiology and pathogenesis.

Topics: Gastrectomy; Gastrins; Humans; Hyperparathyroidism; Peptic Ulcer; Postoperative Complications; Pyloric Stenosis; Stomach Diseases; Vagotomy; Zollinger-Ellison Syndrome

Topics: Adult; Aged; Antacids; Duodenal Ulcer; Female; Gastric Juice; Gastrins; Histamine Antagonists; Humans; Male; Parasympatholytics; Peptic Ulcer; Stomach Ulcer; Zollinger-Ellison Syndrome

Cimetidine, a new histamine H2-receptor antagonist (H.H2.R.A.) is a potent inhibitor of basal and stimulated gastric acid secretion. Contrary to anticholinergics, it does not affect gastric emptying nor does it decrease lower oesophageal sphincter pressure; cimetidine may therefore be used as the treatment of reflux oesophagitis. After prolonged administration of currently used therapeutic doses, basal and post-prandial serum gastrin levels remain unchanged and the parietal cell mass is not increases. Cimetidine toxicity is very low. Cimetidine is effective in promoting healing and pain relief of gastric and duodenal ulcer. In the latter long-term treatment for prevention of relapse is efficient, but the appraisal of its safety remains debated. Efficiency of H.H2.R.A. in the prophylaxis of gastrointestinal haemorrhage in patients with fulminant hepatic failure has been proven. Furthermore, cimetidine has a dramatic ability to control haemorrhage from acute erosive lesions in any seriously-ill patient. It may also be of benefit in the treatment of bleeding from gastric or duodenal ulcer and, whatewer the lesion, in the prevention of bleeding recurrence. In the Zollinger-Ellison syndrome, good results have been obtained but cimetidine treatment must be decided and supervised only by well-informed specialists. Lastly, in patients with severe exocrine pancreatic insufficiency, cimetidine prevents gastric degradation of orally administered pancreatic extracts and decreases steatorrhea.

Topics: Cimetidine; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Guanidines; Humans; Peptic Ulcer; Peptic Ulcer Hemorrhage; Zollinger-Ellison Syndrome

Topics: Animals; Dogs; Gastric Juice; Gastrins; Gastrointestinal Motility; Humans; Pepsin A; Peptic Ulcer; Peptic Ulcer Hemorrhage; Somatostatin; Stomach

Topics: Cimetidine; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Glycoproteins; Humans; Intestinal Mucosa; Peptic Ulcer; Receptors, Histamine; Secretin; Secretory Rate; Somatostatin; Stomach Ulcer; Vasoactive Intestinal Peptide

The familial aggregation of peptic ulcer disease has been well established, as has its association with such clear-cut genetic factors as blood group O and nonsecretor status. However, the genetics of this disorder, or group of disorders, is still in question. Polygenic inheritance is the prevailing hypothesis that has been proposed for peptic ulcer. This hypothesis was based primarily on the exclusion of a simple mode of inheritance for all ulcer disease. Genetic heterogeneity is an alternative hypothesis that can explain both the familial aggregation of peptic ulcer disease and the lack of a simple Mendelian pattern of inheritance. The evidence for genetic heterogeneity in peptic ulcer disease is reviewed, and studies are proposed to test this hypothesis.

Topics: ABO Blood-Group System; Antigens; Chromosome Aberrations; Chromosome Disorders; Duodenal Ulcer; Gastric Juice; Gastrins; Humans; Multiple Endocrine Neoplasia; Pancreatic Neoplasms; Parathyroid Neoplasms; Pepsinogens; Peptic Ulcer; Phenotype; Pituitary Neoplasms; Stomach Ulcer; Werner Syndrome

Topics: Adenoma, Islet Cell; Animals; Diabetes Mellitus; Diarrhea; Gastrins; Glucagon; Humans; Insulin; Insulin Secretion; Islets of Langerhans; Islets of Langerhans Transplantation; Pancreatic Hormones; Pancreatic Neoplasms; Peptic Ulcer; Somatostatin; Transplantation, Homologous

Topics: Achlorhydria; Anemia, Pernicious; Duodenal Ulcer; Gastrectomy; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Liver; Molecular Weight; Peptic Ulcer; Stomach Ulcer; Vagotomy; Zollinger-Ellison Syndrome

Topics: Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Hyperparathyroidism; Paraneoplastic Endocrine Syndromes; Peptic Ulcer; Pyloric Antrum; Radioimmunoassay; Zollinger-Ellison Syndrome

The author made a review about the origin, the biochemistry the physiological and pathological roles of gastrointestinal peptide hormones. They originate from the APUD cell system, chemically from the ancient growth hormone, or placental lactogen. The theoretical prosecgastrin's first sequencies form the "secretin family", the tail sequencies form the "gastrin family". The author describes many details of their effects on the different gastrointestinal organs, they behave mainly antagonistic way to each other. Finally a discussions is given about their role in the development of peptic ulcer, in the WDHA syndrome and in malabsorption.

Topics: APUD Cells; Cell Differentiation; Dumping Syndrome; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Peptic Ulcer; Secretin; Zollinger-Ellison Syndrome

Topics: Duodenum; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Radioimmunoassay; Zollinger-Ellison Syndrome

Topics: Gastrectomy; Gastrins; Humans; Hyperparathyroidism; Pepsinogens; Peptic Ulcer; Vagotomy; Zollinger-Ellison Syndrome

In a short survey recent results of research on gastrin are presented. Special stress is laid upon the mechanism of liberating gastrin, the role of the vagus in this process and the consequences of gastric surgery on serumgastrin. In clinical practice the differential diagnosis of hypergastrinemia in ulcer disease is very important, for it will have a decisive influence on the therapeutic decisions and the specific kind of surgical treatment.

Topics: Duodenal Ulcer; Gastrins; Humans; Peptic Ulcer; Postoperative Complications; Vagotomy; Zollinger-Ellison Syndrome

From 1 to 5% of patients can be expected to develop recurrent ulceration following current surgical therapy for peptic ulcer disease. The development of recurrent ulcer frequently reflects an inadequacy of the initial procedure. The nature of the inadequacy is often difficult to delineate because of alterations in anatomy and physiology and the lack of accurate diagnostic procedures. Incomplete vagotomy and inadequate gastric resection account for the vast majority of surgical deficiencies. Gastrinoma, retained gastric antrum, and hyperparathyroidism are the most frequently encountered endocrine causes. A thorough evaluation must include gastrointestinal X-rays, fiberoptic endoscopy, multiple serum calcium and gastrin determinations, and provocative testing. Medical management of recurrent ulcer fails in the vast majority of cases. Reoperation is successful in about 70% of cases and has a mortality rate of 4%. Recurrent ulcer after simple gastroenterostomy is best treated by gastric resection or vagotomy and resection. After initial adequate gastric resection, vagotomy alone usually suffices. Antrectomy and, if necessary, re-vagotomy should be done for recurrent ulcer after vagotomy and drainage. Re-vagotomy alone is usually effective therapy for recurrent ulcer after initial vagotomy and resection. Non-acid reducing operations should not be done, as they result in high mortality and high second recurrence rates.

Topics: Calcium; Female; Gastrins; Gastroenterostomy; Humans; Hypercalcemia; Male; Pepsinogens; Peptic Ulcer; Recurrence; Vagotomy

Gastric acid secretion by the parietal cell is a single digestive process involving a continuous interplay between nervous and hormonal stimuli. Gastric acid hypersecretion and hypergastrinemia may represent pathologic disturbance of the normal "gastric phase" of acid secretion (excluded antrum syndrome) or abnormal gastrin secretion from a nongastric source as in the Zollinger-Ellison syndrome. Diagnosis of these two syndromes preoperatively is dependent on immunoassay for serum gastrin. A fall in serum gastrin level after the injection of secretin will distinguish the excluded antrum syndrome from the Zollinger-Ellison syndrome. Which hormone or hormones cause the acid hyposecretion of the watery diarrhea hypokalemia achlorhydria syndrome is still uncertain. Potential candidates include secretin, glucagon (alone or combined with gastrin), vasoactive intestinal peptide and gastric inhibitory polypeptide. Secretin has undergone trials as therapy in peptic ulcer whereas glucagon is under investigation for the treatment of acute pancreatitis because of its dual actions as (1) an enterogastrone and (2) an inhibitor of pancreatic secretion.

Topics: Animals; Calcium; Female; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Histamine H1 Antagonists; Humans; Immunoassay; Intestinal Mucosa; Peptic Ulcer; Pyloric Antrum; Rabbits; Secretin; Stimulation, Chemical; Stomach; Swine; Syndrome; Vagus Nerve; Zollinger-Ellison Syndrome

Topics: Animals; Dogs; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Hyperglycemia; Islets of Langerhans; Pancreas; Pancreatitis; Peptic Ulcer; Secretin

Topics: Duodenal Ulcer; Gastrins; Humans; Peptic Ulcer; Stomach; Vagotomy

Topics: 2,2'-Dipyridyl; Animals; Anura; Catecholamines; Cats; Dogs; Gastric Fistula; Gastric Mucosa; Gastrins; Gastrointestinal Agents; Gastrointestinal Hormones; Guinea Pigs; Histamine H1 Antagonists; Histamine Release; Ligation; Pepsin A; Peptic Ulcer; Proglumide; Prostaglandins; Pylorus; Quaternary Ammonium Compounds; Rats; Stomach; Sympatholytics; Thiazoles; Thioacetamide

Topics: Adenoma, Islet Cell; Adolescent; Adult; Aged; Child; Duodenal Neoplasms; Duodenal Ulcer; Female; Gastrectomy; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Neoplasm Metastasis; Pancreatic Neoplasms; Peptic Ulcer; Radiography; Radioimmunoassay; Stomach Neoplasms; Zollinger-Ellison Syndrome

Topics: Acetylcholine; Bicarbonates; Calcium; Cyclic AMP; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Hypercalcemia; Hyperparathyroidism; Pancreatitis; Pepsin A; Peptic Ulcer; Stimulation, Chemical; Vagus Nerve

Topics: Acute Kidney Injury; Adenoma, Islet Cell; Amino Acid Sequence; Animals; Catecholamines; Dehydration; Diarrhea; Duodenal Ulcer; Gastric Juice; Gastrins; Humans; Hyperparathyroidism; Intestinal Mucosa; Peptic Ulcer; Secretory Rate; Stimulation, Chemical; Stomach Ulcer; Syndrome; Zollinger-Ellison Syndrome

Topics: Absorption; Animals; Cyclic AMP; Depression, Chemical; Gastric Juice; Gastric Mucins; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Nicotine; Peptic Ulcer; Prostaglandins; Rats; Secretory Rate; Smoking; Stomach Ulcer

Topics: Anemia, Hypochromic; Body Weight; Bone Diseases; Chronic Disease; Diarrhea; Dumping Syndrome; Duodenal Obstruction; Duodenal Ulcer; Female; Follow-Up Studies; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Insulin; Male; Methods; Pentagastrin; Peptic Ulcer; Peptic Ulcer Hemorrhage; Peptic Ulcer Perforation; Postoperative Complications; Recurrence; Stomach Ulcer; Vomiting

Topics: Digestion; Enzyme Therapy; Fats; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Gastrointestinal Hormones; Humans; Methods; Pancreas; Pancreatectomy; Pancreatic Diseases; Pancreatic Juice; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Duodenal Ulcer; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastrointestinal Motility; Glucose; Histamine; History, 20th Century; Humans; Insulin; Male; Methylene Blue; Nerve Regeneration; Pentagastrin; Pepsin A; Peptic Ulcer; Postgastrectomy Syndromes; Preoperative Care; Pyloric Antrum; Radioimmunoassay; Recurrence; Sex Factors; Stomach; Sympathectomy; Time Factors; Vagotomy

Topics: Angiography; Biological Assay; Diarrhea; Duodenum; Endocrine System Diseases; Gastrectomy; Gastric Juice; Gastrins; Humans; Intestinal Neoplasms; Islets of Langerhans; Malabsorption Syndromes; Pancreatic Neoplasms; Peptic Ulcer; Prognosis; Radioimmunoassay; Stomach; Zollinger-Ellison Syndrome

Topics: Animals; Feedback; Gastric Juice; Gastrins; Humans; Peptic Ulcer; Secretin

Topics: Animals; Duodenal Ulcer; Gastrins; Gastrointestinal Diseases; Humans; Intestine, Small; Liver Cirrhosis; Liver Diseases; Peptic Ulcer

Topics: Age Factors; Amino Acid Sequence; Digestive System; Food; Gastric Juice; Gastrins; Gastrointestinal Motility; Humans; Intestinal Absorption; Pancreas; Peptic Ulcer; Radioimmunoassay; Stomach; Structure-Activity Relationship; Vagus Nerve

Topics: Animals; Calcium; Cholecystokinin; Duodenal Ulcer; Eating; Gastric Mucosa; Gastrins; Histamine; Humans; Islets of Langerhans; Pentagastrin; Pepsin A; Peptic Ulcer; Prostaglandins; Radioimmunoassay; Rats; Secretin; Vagus Nerve

Topics: Animals; Cats; Chronic Disease; Creatinine; Dogs; Duodenal Ulcer; Esophageal Achalasia; Esophageal Diseases; Gastric Mucosa; Gastrins; Gastritis; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Peptic Ulcer; Pyloric Antrum; Rats; Scleroderma, Localized; Stomach Neoplasms; Vagotomy; Zollinger-Ellison Syndrome

Topics: Duodenal Ulcer; Gastrectomy; Gastric Mucosa; Gastrins; Humans; Pepsin A; Peptic Ulcer; Postgastrectomy Syndromes; Postoperative Complications; Stomach Ulcer; Vagotomy; Vagus Nerve

Topics: Anxiety Disorders; Aspirin; Bile Acids and Salts; Blood Group Antigens; Diet; Duodenal Ulcer; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Motility; Histamine; Humans; Hyperplasia; Male; Pentagastrin; Peptic Ulcer; Radioimmunoassay; Stomach Ulcer; Vagotomy

Topics: Drainage; Duodenum; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Postoperative Complications; Pyloric Antrum; Recurrence; Stomach; Vagotomy; Vagus Nerve

Topics: Duodenum; Gastrins; Humans; Jejunum; Peptic Ulcer; Stomach

Topics: Animals; Biogenic Amines; Carcinoid Tumor; Cholecystokinin; Chromaffin System; Diabetes Mellitus; Digestive System; Digestive System Physiological Phenomena; Gastric Juice; Gastrins; Gastrointestinal Hormones; Gastrointestinal Neoplasms; Glucagon; Humans; Insulin; Insulin Secretion; Intestines; Pancreas; Pancreatic Neoplasms; Peptic Ulcer; Secretin; Syndrome

Topics: Calcium; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Hypercalcemia; Hyperparathyroidism; Hypocalcemia; Injections, Intravenous; Peptic Ulcer

Topics: Achlorhydria; Animals; Calcitonin; Calcium; Dogs; Gastric Juice; Gastrins; Glucagon; Humans; Hyperparathyroidism; Magnesium; Parathyroid Glands; Parathyroid Hormone; Peptic Ulcer; Phosphates; Rats

Topics: Dietary Proteins; Duodenal Ulcer; Feedback; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Humans; Male; Peptic Ulcer; Radioimmunoassay; Stomach Ulcer; Vagus Nerve; Zollinger-Ellison Syndrome

Topics: Adenoma; Diagnosis, Differential; Gastrectomy; Gastric Juice; Gastrins; Humans; Neoplasm Metastasis; Peptic Ulcer; Radioimmunoassay; Stomach Neoplasms; Zollinger-Ellison Syndrome

Topics: Biliary Tract Diseases; Ceruletide; Cholangiography; Cholelithiasis; Duodenal Ulcer; Endoscopy; Gastrins; Gastrointestinal Diseases; Gastrointestinal Hemorrhage; Gastrointestinal Hormones; Humans; Intestinal Absorption; Lactose Intolerance; Pancreatic Diseases; Peptic Ulcer; Radionuclide Imaging; Secretin; Stomach Neoplasms

Topics: Anemia, Pernicious; Animals; Diabetes Mellitus; Duodenal Ulcer; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Rats; Secretory Rate; Stomach Ulcer

Topics: Afferent Loop Syndrome; Deglutition Disorders; Diet Therapy; Dumping Syndrome; Gastric Acidity Determination; Gastrins; Gastroenterostomy; Gastroscopy; Humans; Hyperparathyroidism; Malabsorption Syndromes; Pentagastrin; Peptic Ulcer; Postgastrectomy Syndromes; Postoperative Complications; Stomach; Stomach Ulcer; Sutures; Zollinger-Ellison Syndrome

Topics: Anemia, Pernicious; Antibodies; Atrophy; Autoimmune Diseases; Capillaries; Chronic Disease; Dyspepsia; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Hypertrophy; Intrinsic Factor; Metaplasia; Mitosis; Pentagastrin; Pepsin A; Peptic Ulcer; Pyloric Antrum; Radiography; Stomach; Stomach Neoplasms; Thyroid Diseases; Vagotomy

Topics: Bile; Gallbladder; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastrointestinal Motility; Histamine Release; Humans; Intestinal Mucosa; Intrinsic Factor; Muscle, Smooth; Pancreas; Pepsin A; Peptic Ulcer; Pylorus; Zollinger-Ellison Syndrome

Topics: Abdomen; Duodenal Diseases; Duodenal Neoplasms; Duodenal Ulcer; Esophageal Achalasia; Esophageal Diseases; Esophageal Neoplasms; Esophagitis; Esophagoplasty; Esophagus; Female; Gastrins; Gastrointestinal Hemorrhage; Hernia, Diaphragmatic; Humans; Male; Peptic Ulcer; Peptic Ulcer Perforation; Postoperative Complications; Rupture, Spontaneous; Stomach Diseases; Stomach Neoplasms; Stomach Ulcer; Stress, Psychological; Vagotomy

Topics: Aspirin; Atropine; Bile Acids and Salts; Biological Transport; Cell Membrane Permeability; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Hydrochloric Acid; Membrane Potentials; Peptic Ulcer; Potassium; Sodium; Stomach; Vagus Nerve

Topics: Adrenal Cortex Hormones; Animals; Central Nervous System; Gastrins; Graves Disease; Histamine; Humans; Hypertension; Male; Peptic Ulcer; Psychophysiology; Psychosomatic Medicine; Rats; Research

Topics: Animals; Autonomic Nervous System; Cholecystokinin; Dogs; Gastrectomy; Gastrins; Gastroenterostomy; Gastrointestinal Motility; Humans; Peptic Ulcer; Pylorus; Secretin; Vagotomy

Topics: Amino Acid Sequence; Duodenal Ulcer; Feedback; Gastrins; Gastrointestinal Hormones; Humans; Intestinal Absorption; Neurosecretory Systems; Pancreas; Peptic Ulcer; Secretin; Stomach Ulcer; Vagus Nerve; Zollinger-Ellison Syndrome

Topics: Central Nervous System; Cerebral Cortex; Digestion; Duodenal Ulcer; Eating; Emotions; Endopeptidases; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Pepsinogens; Peptic Ulcer; Psychophysiologic Disorders; Stomach; Stomach Ulcer

Topics: Adenoma, Islet Cell; Duodenal Neoplasms; Female; Gastrectomy; Gastrins; Humans; Male; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Colitis, Ulcerative; Gastrins; Gastrointestinal Diseases; Gastroscopy; Humans; Lactose Intolerance; Malabsorption Syndromes; Peptic Ulcer; Stomach Neoplasms

Topics: Air; Anemia, Pernicious; Angiography; Barium; Biopsy; Cholangiography; Colonic Diseases; Contrast Media; Cytodiagnosis; Duodenal Diseases; Endoscopy; Enema; Esophageal Diseases; Gastrins; Gastroenterology; Gastrointestinal Diseases; Gastrointestinal Neoplasms; Gastroscopy; Glucose; Glucuronidase; Gold Isotopes; Insulin; Liver Diseases; Methionine; Pancreatic Diseases; Peptic Ulcer; Peptides; Rectal Neoplasms; Rose Bengal; Selenium; Silicones; Stomach Neoplasms; Vagotomy

Topics: Amino Acid Sequence; Anemia, Pernicious; Animals; Antibodies; Antibody Formation; Chemical Phenomena; Chemistry; Fluorescent Antibody Technique; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Rabbits; Species Specificity; Swine; Zollinger-Ellison Syndrome

Topics: Gastric Acidity Determination; Gastric Juice; Gastrins; Gastrointestinal Hormones; Histamine; Humans; Male; Middle Aged; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Gastric Acidity Determination; Gastric Juice; Gastrins; Gastritis; Histamine; Humans; Inhalation; Intubation, Gastrointestinal; Methods; Peptic Ulcer; Radio; Radioisotopes; Radionuclide Imaging; Stomach; Stomach Neoplasms; Technetium; Vagotomy; Zollinger-Ellison Syndrome

Topics: Amides; Animals; Antiemetics; Atropine; Benzoates; Electromyography; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastrointestinal Motility; Histamine; Humans; Male; Middle Aged; Neostigmine; Peptic Ulcer; Pyrrolidines; Stomach; Stomatitis; Sulfonamides

Topics: Alcohols; Aspirin; Duodenal Ulcer; Female; Gastric Mucosa; Gastrins; Humans; Male; Parasympatholytics; Peptic Ulcer; Peptic Ulcer Perforation; Sex Factors; Steroids; Stomach Ulcer; Stress, Physiological; Stress, Psychological; Time Factors

Topics: Animals; Depression, Chemical; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Liver Cirrhosis; Pancreas; Pancreatic Juice; Pepsin A; Peptic Ulcer; Stimulation, Chemical; Vagus Nerve

Topics: Animals; Dogs; Duodenal Ulcer; Duodenum; Eating; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Pancreas; Pepsin A; Peptic Ulcer; Secretory Rate; Stomach; Vagotomy

Topics: Catecholamines; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Humans; Peptic Ulcer

Topics: Animals; Dogs; Gastric Mucosa; Gastrins; Humans; Liver Cirrhosis; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Animals; Dogs; Gastrins; Humans; Peptic Ulcer; Rabbits

Topics: Antacids; Blood Circulation; Cryosurgery; Duodenal Ulcer; Electrolytes; Gastric Juice; Gastrins; Gastroenterostomy; Gonadal Steroid Hormones; Humans; Insulin; Pancreas; Pathology; Pepsin A; Peptic Ulcer; Pharmacology; Pylorus; Radiation Effects; Radiotherapy; Research; Stomach Ulcer; Stress, Physiological; Vagotomy; Zollinger-Ellison Syndrome

Topics: Gastrins; Gastroenterostomy; Humans; Peptic Ulcer; Physiology; Pyloric Antrum; Vagotomy

Topics: Allergy and Immunology; Blood Group Antigens; Body Constitution; Environment; Gastric Juice; Gastrins; Genetics, Medical; Humans; Peptic Ulcer; Psychology; Stress, Physiological; Vagus Nerve

Roux-en-Y gastric bypass (RYGB) is one of the bariatric surgeries most frequently performed worldwide. Since this operation may predispose to the formation of peptic ulcer of the gastrojejunal anastomosis, the use of proton pump inhibitors (PPI) is recommended during the first postoperative year. However, so far, there is no detailed knowledge about the absorption of this medication during the immediate postoperative period and consequently about its effectiveness in blocking acid secretion. The objective was to assess the possible endoscopic peptic changes, the absorption of omeprazole (OME), and the status of fasting gastrinemia before and after RYGB operation.. OME absorption, the production of its metabolites omeprazole sulfone (OMES) and 5-hydroxyomeprazole (HOME), and basal (fasting) gastrinemia were determined in patients submitted to RYGB before and 2 months after the operation. Upper digestive endoscopy (UDE) was also performed before and 6 months after the operation.. Twenty patients were studied. Preoperatively, all these patients had some peptic changes and 55% tested positive for Helicobacter pylori. Six months after surgery, ten patients still showed endoscopic changes and one patient tested positive for H. pylori. During the postoperative period, there was a reduction of OME absorption and of the production of its metabolites 90 min after administration of the drug, and reduction of serum gastrin levels.. The standard OME dose (40 mg) administered after bariatric surgery is insufficient to achieve serum levels that can effectively block the production of hydrochloric acid, permitting the formation of peptic injuries in many patients.

Topics: Adult; Anastomosis, Roux-en-Y; Fasting; Female; Gastric Bypass; Gastrins; Humans; Male; Middle Aged; Obesity, Morbid; Omeprazole; Peptic Ulcer; Proton Pump Inhibitors

The article presents the results of the first Russian open randomized comparative multicenter study on the effectiveness of Famotidine in the prevention of NSAID-gastropathy--Barrier. In addition, were showen the results of studies of the drugs effect used for prevention of NSAID gastropathy (Famotidine, Lansoprazole, Misoprostol) for the synthesis of prostaglandins in the gastric mucosa in patients with osteoarthritis. Was shown the impact of alternative anti-inflammatory drug on the basis of an extract of ginger as joint pain, and the mucous upper gastrointestinal tract in patients with osteoarthritis.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Anti-Ulcer Agents; Diclofenac; Famotidine; Gastric Mucosa; Gastrins; Humans; Middle Aged; Peptic Ulcer; Prostaglandins; Treatment Outcome

To evaluate the effect of Helicobacter pylori (Hp) eradication therapy on blood gastrin levels in long-term PPI users, since proton pump inhibitors (PPIs) and Helicobacter pylori (Hp) are major causes of hypergastrinaemia.. A prospective study.. Twenty seven Hp (+) patients enrolled in the study. Twenty were given eradication treatment (ET group), and the rest were given symptomatic treatment (ST group). Those who remained Hp (+) after eradication therapy were also added into the ST group. Lansoprazol 30 mg/day was given to both groups for three months thereafter.. Fasting and non-fasting blood gastrin levels (FGL and NFGL) were measured initially and one month and four months after treatment. At the end of fourth month, FGL was significantly higher than both initial and first month level (p < 0.01) in the ST group. NFGL in this group did not change significantly (p > 0.05) after eradication therapy. In the ET group, FGL was significantly higher in the fourth month than the first month (p < 0.001) and than the initial level (p < 0.05). NFGL was higher, but not statistically in the fourth month than in the first month (p > 0.05) and significantly lower than the initial level (p < 0.05) in this group.. We suggest that testing for Hp positivity and treating it if detected would be an appropriate approach to avoid hypergastrinaemia, especially in candidate patients for long term PPI treatment.

Topics: Adult; Anti-Ulcer Agents; Esophagitis; Fasting; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Peptic Ulcer; Prospective Studies; Proton Pump Inhibitors; Time

Pantoprazole is the third proton pump inhibitor to become available. When this study was started, there were few data on its long-term use. Our aim was to investigate this aspect and, because powerful inhibitors of acid secretion can cause hypergastrinemia and, in experimental animals, enterochromaffin-like cell hyperplasia, we also monitored serum gastrin and endocrine cell histology.. One hundred fifty patients refractory to H2-receptor antagonists, running an aggressive course or with complications, were entered into a 5-yr treatment program. We performed serial endoscopy, checked for adverse events, and laboratory values. We also monitored serum gastrin, gastric endocrine cell histology, and antral and corpus gastritis.. This report presents results from up to 3 yr of treatment. Cumulative healing on 40-80 mg of pantoprazole was 82% at 4 wk and 92% by 12 wk. Most patients became asymptomatic within 4 wk. Remission on maintenance treatment with 40 mg (n = 111) was 85% at 12 months and 78% at 24 months. Treatment was safe; only four patients had adverse events definitely related to pantoprazole. Elevations in gastrin were modest and there were no significant changes in gastric endocrine cells. The number of enterochromaffin-like cells tended to decrease.. Pantoprazole is effective, safe, and does not seem to be associated with large increases in serum gastrin or alterations in gastric endocrine cells.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adolescent; Adult; Aged; Anti-Ulcer Agents; Benzimidazoles; Cell Count; Drug Resistance; Enteroendocrine Cells; Enzyme Inhibitors; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Pantoprazole; Peptic Ulcer; Proton Pump Inhibitors; Recurrence; Sulfoxides

Both proton pump inhibitor drug treatment and Helicobacter pylori infection cause hypergastrinaemia in man.. To determine whether eradicating H pylori is a means of reducing hypergastrinaemia during subsequent proton pump inhibitor treatment.. Patients with H pylori were randomised to treatment with either anti-H pylori or symptomatic treatment. One month later, all received four weeks treatment with omeprazole 40 mg/day for one month followed by 20 mg/day for six months. Serum gastrin concentrations were measured before and following each treatment.. In the patients randomised to anti-H pylori treatment, eradication of the infection lowered median fasting gastrin by 48% and meal stimulated gastrin by 46%. When gastrin concentrations one month following anti-H pylori/symptomatic treatment were used as baseline, omeprazole treatment produced a similar percentage increase in serum gastrin in the H pylori infected and H pylori eradicated patients. Consequently, in the patients in which H pylori was not eradicated, median fasting gastrin concentration was 38 ng/l (range 26-86) at initial presentation and increased to 64 ng/l (range 29-271) after seven months omeprazole, representing a median increase of 68% (p < 0.005). In contrast, in the patients randomised to H pylori eradication, median fasting gastrin at initial presentation was 54 ng/l (range 17-226) and was unchanged after seven months omeprazole at 38 ng/l (range 17-95).. Eradicating H pylori is a means of reducing the rise in gastrin during subsequent long term omeprazole treatment. In view of the potential deleterious effects of hypergastrinaemia it may be appropriate to render patients H pylori negative prior to commencing long-term proton pump inhibitor treatment.

Topics: Adult; Alginates; Aluminum Hydroxide; Amoxicillin; Antacids; Anti-Ulcer Agents; Drug Combinations; Drug Therapy, Combination; Esophagitis; Female; Gastrins; Gastroscopy; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Omeprazole; Organometallic Compounds; Peptic Ulcer; Silicic Acid; Sodium Bicarbonate

Omeprazole effectively suppresses acid secretion, resulting in the long-term elevation of intragastric pH and serum gastrin level. Pirenzepine has been reported to inhibit gastrin secretion. This study was carried out to examine the effects of additional pirenzepine treatment on the hypergastrinemia and gastric acid suppression induced by omeprazole. Concentrations of serum gastrin and plasma somatostatin were measured in 28 peptic ulcer patients before treatment, after omeprazole treatment (20 mg/day) for 2 weeks, and after omeprazole and pirenzepine (100 mg/day) treatment for 2 weeks. The acid inhibitory effect of pirenzepine treatment in addition to omeprazole was evaluated by 24-h intragastric pH measurement in six healthy volunteers. Serum gastrin level was increased significantly, to 2.4-fold the pretreatment level, by omeprazole treatment. Additional treatment with pirenzepine suppressed serum gastrin level to 0.6-fold the omeprazole-treatment level. The serum somatostatin level was not altered significantly either by omeprazole treatment or by omeprazole and pirenzepine treatment. In healthy volunteers whose pH 3 holding time on 24-h intragastric pH monitoring was 70% by omeprazole treatment, omeprazole and pirenzepine treatment markedly increased the pH 3 holding time, to 89%. These findings suggest that pirenzepine is useful in reducing the undesirable effects of omeprazole-induced hypergastrinemia, i.e., the excessive trophic effect of omeprazole on the acid-secreting part of the stomach and the overstimulation of acid secretion. The additional pirenzepine treatment is also effective in suppressing acid secretion.

Topics: Adult; Aged; Anti-Ulcer Agents; Drug Therapy, Combination; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Omeprazole; Peptic Ulcer; Pirenzepine; Radioimmunoassay; Somatostatin; Stomach Ulcer

We studied the effects of lansoprazole with or without amoxicillin on the quality of ulcer healing in relation to eradication of Helicobacter pylori. Ulcer healing rates for lansoprazole 30 mg q.d. alone (group A) were 100% for duodenal ulcers (DU; n = 20) and 92% for gastric ulcers (GU; n = 15). The healing rates for lansoprazole 30 mg plus amoxicillin 1-2 g q.d. (group B) were 100% for both DU (n = 20) and GU (n = 12). Endoscopic findings after treatment showed that the red scar/white scar ratio in group A was 16/4 for DU and 12/1 for GU. The red scar/white scar ratio in group B was 4/16 for DU and 6/6 for GU. The numbers of H. pylori in gastric mucus did not change throughout the course of treatment in group A but decreased significantly, without H. pylori relapse, in group B. Changes in ammonia concentration in gastric juice, as well as serum gastrin and pepsinogen I and II levels, differed between group A and group B. Concomitant treatment with lansoprazole and high-dose amoxicillin eradicated H. pylori and modified gastric secretory function, resulting in high-quality ulcer healing.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Amoxicillin; Anti-Ulcer Agents; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Helicobacter pylori; Humans; Lansoprazole; Omeprazole; Penicillins; Pepsinogens; Peptic Ulcer; Proton Pump Inhibitors; Stomach Ulcer

Omeprazole markedly inhibits basal and stimulated gastric acid secretion and has the ability to produce hypergastrinemia and hyperplasia of enterochromaffin-like cells in humans. On the other hand, plaunotol, an acyclic diterpene alcohol, has been reported to inhibit gastrin release by stimulating endogenous secretion release. We investigated the effect of plaunotol on serum gastrin levels after six to eight weeks of omeprazole (20 mg/day) administration in 22 patients (16 males, 6 females; mean age 52.3, range 36-70 years) with peptic ulcer disease. The patients were randomized to the following two groups: 11 subjects with omerprazole alone (single group) and 11 with omeprazole plus plaunotol (240 mg/day) (combination group) treatment. There were no significant differences between the two groups concerning age, sex, ulcer stage, ulcer history, environmental factors, and Helicobacter pylori (HP) prevalence. After complete drug(s) administration, serum immunoreactive (ir) -gastrin levels increased significantly in the single group (P < 0.001) in contrast to the combination group, and plaunotol significantly inhibited hypergastrinemia induced by omeprazole administration (P < 0.001). Significant increases in serum ir-calcitonin gene-related peptide concentrations were observed in the combination group compared to the single group (P < 0.05). However, there were no significant changes in sereum ir-secretin, somatostatin, and vasoactive intestinal polypeptide levels as well as ulcer healing and HP prevalence between the two groups. These findings suggest that plaunotol may suppress hypergastrinemia induced by long-term omeprazole administration, at least partly, via a certain brain-gut hormone affecting gastrin release.

Topics: Adult; Aged; Anti-Ulcer Agents; Diterpenes; Fatty Alcohols; Female; Gastrins; Gastrointestinal Hormones; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer

Fourteen patients subjected to partial gastric resection with vagotomy and a gastroenterostomy (Roux-en-Y, in 11 patients and of Billroth type-II in 3) underwent examinations of the gastric emptying (GE) of a radiolabelled solid meal, as well as of gastric acid and gastrin secretion before surgery and/or within 5.5 weeks postoperatively. The surgery resulted in a significant delay in GE-the median T1/2 nearly doubted from 77 min before to 151 min after the operation (p < 0.01). The GE pattern did not, however, change significantly, as reflected by a median curve shape parameter S amounting to 1.05 and 0.87 before and after the surgery, respectively. The Roux-en-Y reconstruction brought about a pronounced delay in GE with T1/2 exceeding the border of the mean T1/2 + 2SD of healthy controls in 7 (64%) out of 11 patients. On the other hand, no one of the B-II operated patients had a slowed GE. The basal and pentagastrin-stimulated gastric acid secretion was decreased by an average of 71% (from 6.2 +/- 0.7 to 1.8 +/- 0.6 mmol h-1, p < 0.001) and 82% (from 25.2 +/- 3.0 to 4.4 +/- 1.2 mmol h-1, p < 0.001), respectively. The surgery did not affect the fasting serum gastrin concentration (53.2 +/- 4.9 pre- vs 51.0 +/- 11.5 ng.l-1 postoperatively), whereas the postprandial gastrin release decreased significantly-AUC0-120: 9838 +/- 1377 ng.l-1 min before and 6863 +/- 1024 ng.l-1 min after the operation, p < 0.01.

Topics: Adult; Anastomosis, Roux-en-Y; Female; Gastrectomy; Gastric Acid; Gastric Emptying; Gastrins; Gastroenterostomy; Humans; Male; Middle Aged; Peptic Ulcer; Postoperative Period; Radionuclide Imaging; Vagotomy, Truncal

Gastric emptying (GE) of a radiolabelled solid meal, gastric acid secretion and gastrin release was measured before and/or by 91/2 weeks postoperatively in 12 patients with partial gastric resection supplied with Billroth-I gastroduodenoanastomosis and usually (n = 10) with truncal vagotomy [B-1+(VT))]. The results obtained were compared to those derived from another study involving 14 patients with partial gastric resection supplied with a gastroenterostomy (of Roux-en-Y type in 11, and Billroth-II type in 3 subjects) and truncal vagotomy [Roux(B-II)+VT]. The B-I+(VT) procedure affected significantly neither the overall GE (the median T1/2 was 75 min before and 95 min after the surgery) nor the GE pattern-the median curve shape parameter S was 0.73 before and 1.07 after the operation. The basal and pentagastrin-stimulated gastric acid secretion was reduced by an average of 79% (from 8.6 +/- 2.5 to 1.8 +/- 0.5 mmol h-1, p < 0.05) and 77% (from 22.0 +/- 2.8 to 5.0 +/- 1.5 mmol h-1, p < 0.05) after the B-I+(VT), respectively. Moreover, after the B-I+(VT) a decrease in the fasted serum gastric concentration (78.3 +/- 17.0 before vs 62.4 +/- 6.9 ng l-1 after the surgery) and in the postprandial gastrin release (AUC0-120: 11716 +/- 2482 ng l-1 min before vs 9753 +/- 1183 ng l-1 min after the surgery) was found; the relevant differences were, however, statistically not significant. In patients with a preoperatively normal GE, a markedly slowed GE (T1/2 above the limit of the mean T1/2 +2SD in healthy controls) was found in 5 out of 8 (62%) patients after the Roux-en-Y procedure, and only in 1 out of 7 (14%) patients after the B-I or B-II procedure. With regard to the postoperative data, the Roux (B-II)+VT resulted in lower gastric acid secretion and gastrin release than the B-I+(VT) procedure but the relevant differences were statistically not significant.

Topics: Adult; Anastomosis, Surgical; Duodenum; Gastrectomy; Gastric Acid; Gastric Emptying; Gastrins; Gastroenterostomy; Humans; Male; Middle Aged; Peptic Ulcer; Postoperative Period; Radionuclide Imaging; Stomach; Vagotomy, Truncal

Serum gastrin levels in 44 peptic ulcer patients (26 gastric ulcer patients and 18 duodenal ulcer patients) were determined after they had been treated with omeprazole (OPZ) (20 mg/day) alone or in combination with pirenzepine (PZP) (100 mg/day). Serum gastrin levels were measured before, as well as 2, 4, and 6 weeks after administration, and the changes were compared. The levels were significantly elevated (twofold) at 2 weeks of treatment in both the OPZ and OPZ plus PZP groups. In patients taking OPZ alone, the levels rose up to 6 weeks, while in those taking OPZ plus PZP the levels decreased at 4 and 6 weeks. At 4 weeks, serum gastrin levels in the OPZ plus PZP group were lower (although not significantly) than those in patients taking OPZ alone. In gastric ulcer patients, serum gastrin levels in the OPZ group were significantly elevated, while in the OPZ plus PZP group, these levels were only slightly, but not significantly elevated. There was no significant difference between the two gastric ulcer groups at any time. In duodenal ulcer patients, serum gastrin levels increased significantly at 2 weeks of treatment in both groups. At 4 weeks and thereafter, the serum gastrin levels remained significantly high in patients taking OPZ alone, while they decreased at both 4 and 6 weeks in patients taking OPZ plus PZP. Thus, serum gastrin levels in duodenal ulcer patients were markedly decreased by the addition of PZP.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Drug Therapy, Combination; Duodenal Ulcer; Gastrins; Humans; Omeprazole; Peptic Ulcer; Pirenzepine; Stomach Ulcer

To verify the effect of age on gastric secretions in gastric (GU) and duodenal ulcer (DU) patients, we carried out a retrospective study evaluating basal and stimulated gastric acid secretion in 427 peptic ulcer subjects aged between 12 and 73 years (GU = 74, DU = 353) in addition to studying gastric juice pepsin, serum pepsinogen group A (PGA) and gastrin in 175 patients (GU = 28, DU = 147). All subjects were then divided into groups according to their sex and age (< 30, 30-39, 40-49, 50-59 and > 60 years). Basal, maximal and peak acid outputs (BAO, MAO, PAO) were unchanged in the various age groups, though MAO and PAO were higher in males than females and in DU than in those with GU, even in the elderly (> 60 years). Pepsin and gastrin levels were unchanged at the various ages in GU and DU, while PGA was higher in males with DU aged 50 or over. This demonstrates that acid, pepsin and gastrin secretions do not change with age in ulcer patients. Acid secretion retains its typical distribution according to pathology (DU > GU) and sex (males > females), and also appears to have a fundamental pathogenetic role in peptic ulcer in the elderly.

Topics: Adolescent; Adult; Aged; Aging; Child; Duodenal Ulcer; Female; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Pentagastrin; Pepsin A; Pepsinogens; Peptic Ulcer; Retrospective Studies; Stomach Ulcer

Patients (106) with peptic ulceration of the oesophagus, stomach and duodenum, unresponsive to 3 or more months of high-dose treatment with ranitidine, were initially given pantoprazole (40-80 mg, p.o.) daily. In 96.7% of the patients ulcers healed within 2 to 8 weeks, and in 2.3% of patients the ulcers healed within 12 weeks. In just one patient with severe oesophagitis, the lesion took more than 6 months to heal. After ulcer healing, patients (98 to date) were treated with pantoprazole (40 mg/day) as long-term maintenance therapy. Eighty-eight of the 98 patients have been taking pantoprazole for 6 months to 3 years. During maintenance therapy, peptic disease was kept in remission in most patients with 40 mg pantoprazole. Twelve patients with oesophagitis and two patients with gastric ulcers needed higher doses (80-120 mg) to control the disease. One female patient developed peripheral oedema which disappeared quickly after stopping treatment. No further drug-related adverse effects were observed. Seven patients withdrew from the study and two patients died, all for non-drug-related reasons. Routine laboratory tests remained without significant changes in all patients. Mean (+/- S.E.M.) serum gastrin levels were already elevated during the initial high-dose ranitidine treatment (128 +/- 23 pg/ml). Within one year of the start of the pantoprazole treatment, serum gastrin levels rose to 3 times normal values (189 +/- 32 pg/ml). Thereafter, no further increases in serum gastrin were observed for up to 2.5 years. Enterochromaffin-like (ECL) cell density increased very slightly from 0.19% to 0.24% within one year.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Benzimidazoles; Duodenal Ulcer; Enterochromaffin Cells; Esophagitis; Female; Gastrins; Humans; Longitudinal Studies; Male; Omeprazole; Pantoprazole; Peptic Ulcer; Proton Pump Inhibitors; Ranitidine; Stomach Ulcer; Sulfoxides

The effects of oral indomethacin on intragastric pH and serum gastrin were investigated in rheumatoid arthritis patients. Nine patients (1 male, 8 female) without a history of peptic ulcer disease and 6 patients with a history of peptic ulcer disease (5 male, 1 female) were studied. To obviate Helicobacter pylori infection as a confounding factor, only patients with positive H. pylori serology were included. After a 5-day period of placebo treatment and after a 5-day period of indomethacin (50 mg t.d.s.; total dose 750 mg), 24-h intragastric pH and basal and meal-stimulated serum gastrin levels were measured in a double-blind placebo controlled cross-over study. There were no differences in the median 24-h pH values between placebo and indomethacin users irrespective of peptic ulcer disease history. Indomethacin resulted in a higher basal and stimulated gastrin response than placebo in patients with a history of peptic ulcer disease. The basal and incremental responses were lower in patients with a history of peptic ulcer disease than in patients without a history of peptic ulcer disease, both during indomethacin and placebo. The same basal and stimulated incremental serum gastrin responses were found during placebo and indomethacin treatment in patients without a history of peptic ulcer disease. No correlation was established between median 2-h post-prandial intragastric pH and post-prandial incremental serum gastrin concentration. We conclude that indomethacin does not influence the intragastric pH of rheumatoid arthritis patients irrespective of history of peptic ulcer disease.

Topics: Administration, Oral; Aged; Arthritis, Rheumatoid; Basal Metabolism; Double-Blind Method; Female; Food; Gastric Acidity Determination; Gastrins; Humans; Hydrogen-Ion Concentration; Indomethacin; Male; Middle Aged; Monitoring, Physiologic; Peptic Ulcer

A randomized prospective study on the response of fasting serum gastrin concentrations in peptic ulcer patients was performed in order to test the hypothesis that H. pylori infection in the gastric antrum increases gastrin release, and to examine whether the high fasting serum gastrin concentrations respond to treatment that eradicates H. pylori.. One hundred and twenty-seven patients with gastric or duodenal ulcer were included in this study. Patients were divided into three groups on the basis of antral H. pylori status and therapeutic modalities. The first group, 58 patients infected by H. pylori, was treated with metronidazole and tripotassium dicitrato bismuthate combined with ranitidine and mylanta. The second group, 40 patients also infected by H. Pylori, was treated with ranitidine and mylanta. The third group, 29 patients, free of H. pylori infection, was designed to evaluate the influence of H2-receptor antagonist on the change of gastrin. When ulcers were completely healed, changes of gastrin concentrations and H. pylori status were re-examined.. H. pylori was eradicated in all patients who have received antibacterial therapy in 4 weeks, and serum gastrin concentrations were significantly decreased after eradication of the organism both in gastric and in duodenal ulcer diseases. (Gastric ulcer: 129.3 +/- 47.0 pg/ml before and 63.7 +/- 21.6 pg/ml after treatment. Duodenal ulcer: 108.3 +/- 35.0 pg/ml and 66.5 +/- 21.9 pg/ml, respectively. Total: 112.7 +/- 38.2 pg/ml vs 66.0 +/- 21.6 pg/ml) (p < 0.01). In contrast, H. pylori-positive patients who have not received antibacterial therapy were still infected at the completion of the study, and serum gastrin concentrations increased even though the difference was not significant. (Gastric ulcer: 118.4 +/- 51.2 pg/ml vs 124.0 +/- 56.5 pg/ml. Duodenal ulcer: 85.4 +/- 35.1 pg/ml vs 104.6 +/- 43.5. Total: 99.5 +/- 45.3 vs 112.9 +/- 48.7 pg/ml.) (p > 0.05). None of the patients who were initially H. pylori-negative has been reinfected during the period of the study, and their serum gastrin concentrations were not changed. (Gastric ulcer: 69.8 +/- 38.0 pg/ml. Total: 63.2 +/- 31.1 pg/ml. Duodenal ulcer: 55.1 +/- 17.6 pg/ml vs 55.8 +/- 13.8 pg/ml. Total: 63.2 +/- 31.1 pg/ml vs 63.4 +/- 30.0 pg/ml). Four- to six-week therapy of H2-receptor antagonist and antacid had no influence on serum gastrin concentrations.. On the basis of the above results, we confirmed that the chronic infection of H. pylori of gastric antrum in peptic ulcer patients causes increased release of serum gastrin, and eradication of the organism results in a significant fall in serum gastrin concentrations.

Topics: Adolescent; Adult; Aged; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Peptic Ulcer; Prospective Studies; Pyloric Antrum; Stomach Diseases

Forty-two patients with peptic ulceration of the duodenum, stomach or oesophagus, who had not responded to 3 or more months of high-dose treatment with ranitidine (450 or 600 mg/day), were treated with oral lansoprazole at 30-60 mg daily. In 40 patients (95.2%) the ulcers healed within 2-12 weeks. In the remaining 2 patients healing took several months but eventually all ulcers healed. After healing, 40 patients underwent long-term maintenance treatment with 30-60 mg lansoprazole daily for 1-3 years (continuing). During maintenance therapy with lansoprazole, no endoscopically verified relapses occurred when the drug was taken regularly. In 1 patient treatment had to be discontinued because of a drug-related colitis that disappeared soon after treatment had been stopped. There were no significant changes in routine laboratory tests in any patient. Basal serum gastrin concentrations, which were already elevated by the previous high-dose ranitidine treatment (125 +/- 25 pg/ml), rose to four times the normal values after 4 weeks of treatment with lansoprazole (255 +/- 65 pg/ml). Thereafter no further increases in basal serum gastrin concentrations were observed, even after 3 years of administration. The volume density of argyrophilic cells in the oxyntic mucosa increased slightly during lansoprazole treatment; until now no dysplasia of the enterochromaffin-like cells has been observed. In conclusion, 30-60 mg lansoprazole daily healed ranitidine-resistant peptic ulcers, and subsequent maintenance therapy with 30-60 mg lansoprazole daily was found to be highly effective and safe over the time observed.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Anti-Ulcer Agents; Dose-Response Relationship, Drug; Drug Administration Schedule; Drug Resistance; Duodenal Ulcer; Enterochromaffin Cells; Esophagitis; Female; Follicle Stimulating Hormone; Gastric Mucosa; Gastrins; Humans; Lansoprazole; Luteinizing Hormone; Male; Omeprazole; Peptic Ulcer; Pyloric Antrum; Ranitidine; Stomach Ulcer; Testosterone

Since the Roux-en-Y anastomosis prevents the sequela of postoperative enterogastric reflux after gastrectomy, this approach has been advocated as the primary procedure in patients undergoing gastrectomy for peptic ulcer. We have prospectively followed for 2 years 22 patients, in whom gastrectomy was performed with, at random, either Roux-en-Y (n = 11) or Billroth II (n = 11) anastomosis. Two of the 11 patients who had received the Roux-en-Y procedure had anastomotic ulcers, leading to reresection in one of them. These two patients were found to have the highest values for basal and pentagastrin stimulated gastric acid output. After the Billroth II procedure a single patient had a small anastomotic ulcerative lesion. Apart from differences in intragastric bile acids (p less than 0.0001) and the gastritis activity score (p less than 0.01), no significant differences were found between the patients with Roux-en-Y and Billroth II anastomosis with respect to basal and pentagastrin-stimulated gastric acid secretion, basal, postprandial and bombesin-stimulated serum gastrin secretion, serum pepsinogen A and C concentrations, the serum pepsinogen A/C ratio, postprandial glucose, and for a modified Visick grading. From this small series we conclude that, as compared with the Billroth II-anastomosis, the Roux-en-Y procedure effectively prevents enterogastric reflux, and is associated with a higher gastritis activity score, but not with differences in gastric acid, gastrin, pepsinogens, or Visick grading. Furthermore, inadequate reduction of acid secretion in some patients after the Roux-en-Y procedure may lead to recurrent peptic ulcers.

Topics: Anastomosis, Roux-en-Y; Anastomosis, Surgical; Bile Acids and Salts; Duodenal Ulcer; Female; Gastrectomy; Gastric Acid; Gastrins; Humans; Jejunum; Male; Middle Aged; Peptic Ulcer; Prospective Studies; Random Allocation; Recurrence

In order to delineate the role of enterogastric reflux in changes of postoperative gastric secretory functions, 22 patients with peptic ulcers, who were randomly assigned to partial gastrectomy without vagotomy with either Billroth II or Roux-en-Y anastomosis, were prospectively studied before and 6 months after surgery. Preoperatively, there were no significant differences in gastric secretory functions between the two groups of 11 patients. Postoperatively, median fasting bile acids in the stomach increased in the Billroth II patients from 0.35 to 16.10 mumol/hr (p less than 0.01), but significantly decreased in the Roux-en-Y patients from 0.30 to 0.10 mumol/hr (p less than 0.05), which indicated adequate prevention of enterogastric reflux after the Roux-en-Y procedure. Gastrectomy resulted in significant reductions of median values of basal acid output (4.6 vs 0.6 mmol/hr, p less than 0.01, and 4.2 vs 0.4 mmol/hr, p = 0.02), peak acid output (31.6 vs 4.2 mmol/hr, p less than 0.01, and 38.7 vs 4.5 mmol/hr, p less than 0.01), serum pepsinogen A (121 vs 86 micrograms/L, p less than 0.01, and 92 vs 45 micrograms/L, p less than 0.01), meal-stimulated serum gastrin secretion (1472 vs 199 pM.60 min, p less than 0.0001, and 1017 vs 199 pM.60 min, p less than 0.0001) in the patients with Billroth II and Roux-en-Y anastomosis, respectively. There were, however, no significant differences in gastric secretory parameters between the two groups when studied 6 months after surgery. Therefore it is concluded that after gastrectomy, enterogastric reflux does not affect the secretory function of the gastric remnant within the first 6 months after surgery.

Topics: Anastomosis, Roux-en-Y; Anastomosis, Surgical; Bile Acids and Salts; Bile Reflux; Biliary Tract Diseases; Eating; Fasting; Female; Gastrectomy; Gastric Acid; Gastrins; Humans; Male; Middle Aged; Pepsinogens; Peptic Ulcer; Prospective Studies

Roxatidine acetate is a novel H2-receptor antagonist with a chemical structure different to the earlier drugs of this type. It is a potent inhibitor of histamine-mediated gastric acid secretion and in animal models is 4 to 6 times as potent as cimetidine. In a multicentre double-blind clinical trial of over 700 patients with gastric or duodenal ulcers roxatidine acetate 75 mg twice daily and cimetidine 200mg four times daily produced endoscopically confirmed and subjective and objective healing rates in excess of 90% for both types of ulcer, with no significant difference between the treatments. Roxatidine acetate's efficacy in stomal ulcer (marginal ulcer) and reflux oesophagitis has been confirmed in non-comparative studies of up to 8 weeks' duration. The overall incidence of adverse reactions in 1623 patients treated with roxatidine acetate 75 mg twice daily was 1.7%, with skin rashes and constipation the most frequently reported side effects.

Topics: Adult; Cimetidine; Duodenal Ulcer; Female; Gastrins; Histamine H2 Antagonists; Humans; Japan; Male; Middle Aged; Pepsinogens; Peptic Ulcer; Piperidines; Prolactin; Stomach Ulcer; Time Factors

The efficacy of cimetidine, 1.2 and 2.4 g/day, compared to placebo treatment given in addition to conventional therapy, which included antacids, in the prevention of gastroduodenal lesions associated with stress in 105 patients with acute spinal injury was investigated. Haematemesis was only observed in 1 placebo-treated patient. Of the 84 patients who completed the 10-day treatment and underwent endoscopy, 12 out of 43 cimetidine-treated patients and 11 out of 41 patients who received placebo were found to have gastroduodenal ulceration and/or erosions. Mean circulating concentrations of gastrin, pancreatic polypeptide and secretin were similar in all groups of patients. Whilst cimetidine has been shown to reduce the incidence of ulceration in patients suffering cranial and thermal injuries, the present study failed to demonstrate a prophylactic effect of cimetidine in the primary prevention of ulcers or erosions in patients with acute spinal injury exceeding that of conventional antacid therapy.

Topics: Adolescent; Adult; Aged; Cimetidine; Clinical Trials as Topic; Dose-Response Relationship, Drug; Double-Blind Method; Drug Therapy, Combination; Female; Gastrins; Humans; Male; Middle Aged; Pancreatic Polypeptide; Peptic Ulcer; Risk; Secretin; Spinal Cord Injuries; Stress, Physiological

The effectiveness of cimetidine or antacid in healing recurrent jejunal peptic ulcers after Billroth II gastric resection without vagotomy was tested in a randomized study of 18 in-patients. Mean stimulated acid secretion of the cimetidine group was 11.2 +/- 4.3 mmol/h, in the antacid group 12.6 +/- 5.6 mmol/h. Serum gastrin levels were within the normal range in all patients. Within four weeks the ulcers had healed completely in eight of the nine patients on cimetidine (1,000 mg/d), but in only three of the nine patients on antacids (magnesium-aluminiumhydroxide, neutralization capacity 564 mmol/d). The difference is statistically significant (P less than 0.025). All 11 patients with healed ulcers were given prophylactically either 800 mg cimetidine daily or magnesium-aluminiumhydroxide (neutralization capacity 564 mmol/d). During a follow-up period of one year recurrences occurred in two of the five patients on antacids, but in none of the six treated with cimetidine. The results indicate that cimetidine also accelerates the healing of recurrent jejunal peptic ulcers. But further studies are required to elucidate whether long-term treatment with histamine-H2-receptor antagonists is as good as surgery in the long-term prevention of ulcer recurrences.

Topics: Adult; Antacids; Cimetidine; Female; Gastrectomy; Gastrins; Guanidines; Humans; Jejunal Diseases; Male; Middle Aged; Peptic Ulcer; Postoperative Complications; Recurrence

Calcitonin (CT) inhibits basal and pentagastrin stimulated gastric acid and pepsin secretion by 60 to 70% when CT is infused over a short period of time. Vagal and histamine-mediated stimulations are less diminished. A long-term infusion of CT inhibits persitently basal and pentagastrin-stimulated acid and pepsin secretion over more than 24 hours in patients with duodenal ulcer, stress bleeding and Zollinger-Ellison-Syndrome. To date, the therapeutic efficiency of CT in gastroduodenal bleeding has not been evaluated in a controlled trial. CT inhibits gastric secretion also after oral application. In an endoscopically controlled double blind trial we were not able to demonstrate a significant benefit of oral CT in patients with gastric ulcer. In ulcer bleeding CT does not apear reasonable in comparison with histamine-H2-receptor antagonists which apparently is more efficient and less costly.

Topics: Calcitonin; Clinical Trials as Topic; Double-Blind Method; Gastric Juice; Gastrins; Humans; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Antacids; Anti-Ulcer Agents; Bismuth; Carbenoxolone; Cimetidine; Clinical Trials as Topic; Costs and Cost Analysis; Gastric Juice; Gastrins; Humans; Parasympatholytics; Peptic Ulcer; Recurrence

Topics: Adult; Cimetidine; Clinical Trials as Topic; Double-Blind Method; Endoscopy; Female; Fiber Optic Technology; Gastric Juice; Gastrins; Guanidines; Humans; Male; Middle Aged; Peptic Ulcer; Placebos; Random Allocation; Recurrence; Time Factors

Parietal cell vagotomy has been in clinical use for 7 years in elective treatment of nonobstructive duodenal ulcer, and for even a shorter period for complicated cases and for gastric ulcer The evolution of the surgical technique has not yet come to an end and the ability to perform the procedure is still improving. It can therefore be questioned, if this operation is yet ripe for a realistic clinical trial, and the great variation in recurrence rate reported in pilot series as well as in prospective randomized clinical trials points to the possibility that we will have to wait several years before the anticipated mean recurrence rate is known. At present it can be stated that even if gastric emptying is not quite undisturbed, the addition of a drainage procedure in nonobstructive cases is unnecessary. The same may be true in some patients with pyloric obstruction. Furthermore, the mortality rate is very low and the incidence of moderate-to-severe dumping and diarrhea is virtually nil.

Topics: Animals; Clinical Trials as Topic; Denmark; Diarrhea; Drainage; Dumping Syndrome; Duodenal Ulcer; Gastric Juice; Gastrins; Gastrointestinal Motility; Humans; Peptic Ulcer; Pilot Projects; Postoperative Complications; Pyloric Stenosis; Recurrence; Stomach; Stomach Ulcer; Vagotomy

In a prospective clinical study, 100 seriously ill patients were investigated in regard to the risk of stress ulcer. It could be shown that raised shock indices with simultaneous low hemoglobin, hematocrit, albumin and serum calcium levels, as biologically measurable quantities, suggest a danger of stress ulcer.

Topics: Adult; Calcium; Clinical Trials as Topic; Critical Care; Female; Gastric Juice; Gastrins; Hematocrit; Hemoglobins; Humans; Male; Middle Aged; Peptic Ulcer; Prospective Studies; Serum Albumin; Shock; Stress, Physiological

Topics: Adolescent; Adult; Aged; Benzamides; Clinical Trials as Topic; Drug Evaluation; Duodenal Ulcer; Female; Gastrins; Gastritis; Gastrointestinal Agents; Glutarates; Humans; Male; Middle Aged; Peptic Ulcer; Stomach Ulcer

Topics: Adolescent; Adult; Aged; Clinical Trials as Topic; Dyspepsia; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Histamine; Humans; Injections, Subcutaneous; Male; Middle Aged; Peptic Ulcer; Secretory Rate; Stomach Neoplasms

Topics: Colon; Colon, Sigmoid; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastrointestinal Motility; Histamine; Humans; Injections, Intramuscular; Injections, Intravenous; Intestinal Diseases; Peptic Ulcer; Pylorus; Pyrazoles; Rectum; Stomach

Gastrinoma may cause refractory esophageal stricture due to gastro-esophageal reflux disease (GERD), but imaging technologies have limited power in its diagnosis. A 74-year-old female with a history of peptic ulcers suffered from repeated epigastralgia, and she visited a local hospital. An esophago-gastro-duodenoscopy (EGD) demonstrated severe reflux esophagitis and multiple peptic ulcers. Blood examination revealed a high value of fasting serum gastrin. Multi-detector computed tomography showed a hypervascular and tiny nodule in duodenal bulb, although other imaging technologies did not. Short-term medication with a proton pump inhibitor or potassium-competitive acid blocker was intermittently provided, but dysphagia was repeatedly worsened, and she was referred to our division. Serum hypergastrinemia was retained, and EGD reexamination depicted esophageal stricture, treated by multiple sessions of endoscopic balloon dilatation. Primary tumor was not identified by the morphological imaging technologies, but a selective arterial secretagogue injection test suggested its existence in the duodenum or pancreatic head. Pancreaticoduodenectomy was performed, and histological study identified 2 mm-sized microgastrinoma buried in Brunner`s glands on the posterior wall of the duodenum bulb. We reported a case with difficulty in diagnosis of the smallest sporadic gastrinoma of the duodenum, which might cause refractory GERD-associated stricture.

Topics: Aged; Duodenum; Esophageal Stenosis; Female; Gastrinoma; Gastrins; Gastroesophageal Reflux; Humans; Pancreatic Neoplasms; Peptic Ulcer; Potassium; Proton Pump Inhibitors; Secretagogues

Peptic ulcer disease is a frequent clinical problem with potentially serious complications such as bleeding or perforation. A decisive factor in the pathogenesis of peptic ulcers is gastric acid, the secretion of which is controlled by the hormone gastrin released from gastric G cells. However, the molecular mechanisms regulating gastrin plasma concentrations are poorly understood. Here, we identified a semaphorin-plexin signaling pathway that operates in gastric G cells to inhibit gastrin expression on a transcriptional level, thereby limiting food-stimulated gastrin release and gastric acid secretion. Using a systematic siRNA screening approach combined with biochemical, cell biology, and in vivo mouse experiments, we found that the RasGAP protein Rasal1 is a central mediator of plexin signal transduction, which suppresses gastrin expression through inactivation of the small GTPase R-Ras. Moreover, we show that Rasal1 is pathophysiologically relevant for the pathogenesis of peptic ulcers induced by nonsteroidal anti-inflammatory drugs (NSAIDs), a main risk factor of peptic ulcers in humans. Last, we show that application of recombinant semaphorin 4D alleviates peptic ulcer disease in mice in vivo, demonstrating that this signaling pathway can be harnessed pharmacologically. This study unravels a mode of G cell regulation that is functionally important in gastric homeostasis and disease.

Topics: Animals; Cell Adhesion Molecules; Gastrins; GTPase-Activating Proteins; Humans; Mice; Nerve Tissue Proteins; Peptic Ulcer; Semaphorins; Signal Transduction

Neurofibromatosis type (NF-1) is an autosomal dominant disorder characterized predominantly by neurocutaneous manifestations. Involvement of the gastrointestinal tract is uncommon but is associated with a significant risk of malignancy. There are a handful of case reports linking NF-1 with pancreatic neuroendocrine tumors; these include gastrin-secreting variants with the attendant Zollinger-Ellison syndrome. We present the case of a 52-year-old lady who presented with recurrent peptic ulceration and diarrhea. Serum gastrin levels were elevated and magnetic resonance imaging demonstrated the presence of a pancreatic lesion with multiple liver metastases. The lesion was moderately fludeoxyglucose avid on positron emission tomography-computed tomography. Endoscopic ultrasonography-guided sampling revealed the presence of synaptophysin positive neuroendocrine cells with positive gastrin immunostaining. A conservative approach was adopted, and the patient's symptoms improved on proton pump inhibitors. Zollinger-Ellison syndrome is an important condition, which should be kept in mind in the patient with NF-1 who presents with recurrent peptic ulceration and diarrhea. The emerging association between these 2 conditions is being examined on a cellular and immunohistochemical level.

Topics: Diarrhea; Female; Gastrinoma; Gastrins; Humans; Middle Aged; Neuroendocrine Tumors; Neurofibromatosis 1; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

The present study was designed to observe the effect of quadruple therapy combined with probiotics on

Topics: Amoxicillin; Anti-Bacterial Agents; Bismuth; Drug Therapy, Combination; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Metronidazole; Motilin; Pectins; Peptic Ulcer; Probiotics; Proton Pump Inhibitors; Somatostatin; Tablets, Enteric-Coated

Methods for the measure of gastric acid secretion include invasive and non-invasive tests. The gold-standard to measure the acid output is the collection of gastric after in basal condition (Basal Acid Output, B.A.O.) and after an i.m. injection of pentagastrin (Maximal Acid Output, M.A.O.). However, direct measurement of gastric acid production is out of order in clinical practice, but many GI symptoms are claimed to be related with acid disorders and empirically cured. Hypochlorhydria is associated with precancerous conditions such as chronic atrophic gastritis (CAG). Acid measurement with non-invasive methods (pepsinogens) is supported by international guidelines.

Topics: Achlorhydria; Biomarkers; Gastric Acid; Gastric Acidity Determination; Gastrins; Gastritis, Atrophic; Humans; Pentagastrin; Pepsinogens; Peptic Ulcer; Precancerous Conditions

The symptomatic presentation of Meckel's diverticulum (MD) depends on a person's age, sex, and presence or absence of ectopic gastric tissue. There are no differences in the prevalence of asymptomatic MD between males and females; however, symptomatic MD has a distinct male predominance with a male-to-female ratio ranging from 2:1 to 5:1 in children. Furthermore, if the ectopic tissue contains gastric mucosa, MD has a greater chance of becoming symptomatic. Studies have shown that acid secretion is more likely to occur in male infants compared to female infants. In adults, men are known to have a higher level of acid production compared to women. Peptic ulcers (PU) are more common in males due to high acid secretion, and gastric tissues are affected by gastrin secretion in both conditions. MD is typically accompanied by ectopic gastric tissue, and could therefore be affected by gastrin and acid secretion in a similar manner to PU. Some of the major complications of MD are diverticulitis, ulcers, and bleeding from adjacent ectopic gastric tissue, and such complications resemble PU. PU also have male to female ratios ranging from 2:1 to 5:1, which is again similar to MD. Since the secretion of both gastrin and acid decrease with age, symptomatic presentation of MD also declines with age. Therefore, we hypothesize that higher gastrin and acid levels in males affect the ectopic gastric mucosa and lead to an increase in MD symptoms, which result an increased incidence of MD in males.

Topics: Adolescent; Age Factors; Child; Child, Preschool; Choristoma; Female; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Infant; Infant, Newborn; Male; Meckel Diverticulum; Models, Theoretical; Peptic Ulcer; Sex Factors; Vitelline Duct

Toll-like receptor 4 is a part of the innate immune system and recognizes Helicobacter pylori lipopolysaccharide. The goal of this study was to analyze the role of Toll-like receptor 4 polymorphisms +896 (rs4986790) and +1196 (rs4986791) in the pathogenesis of Helicobacter pylori related gastroduodenal diseases in relation to gastric secretion and inflammation. Toll-like receptor 4 polymorphisms, serum gastrin-17 and pepsinogen I and II concentrations were determined, and gastroscopies with histopathological analyses were performed to 216 dyspeptic patients. As genotype controls, 179 controls and 61 gastric cancer patients were studied. In our study, the Toll-like receptor 4 +896 and +1196 polymorphisms were in total linkage disequilibrium. The homozygous wild types displayed higher gastrin-17 serum concentrations than the mutants (p = 0.001) and this effect was independent of Helicobacter pylori. The homozygous wild types also displayed an increased risk for peptic ulcers (OR: 4.390). Toll-like receptor 4 genotypes did not show any association with Helicobacter pylori positivity or the features of gastric inflammation. Toll-like receptor 4 expression was seen in gastrin and somatostatin expressing cells of antral mucosa by immunohistochemistry. Our results suggest a role for Toll-like receptor 4 in gastric acid regulation and that the Toll-like receptor 4 +896 and +1196 wild type homozygozity increases peptic ulcer risk via gastrin secretion.

Topics: Adult; Aged; Aged, 80 and over; Female; Gastrins; Gastritis; Gene Frequency; Genetic Predisposition to Disease; Genotype; Helicobacter Infections; Helicobacter pylori; Humans; Immunohistochemistry; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Peptic Ulcer; Polymorphism, Single Nucleotide; Risk Factors; Stomach Neoplasms; Toll-Like Receptor 4; Young Adult

Physiology of gastric acid secretion is one of the earliest subjects in medical research and education. Gastric acid secretion has been sometimes inadequately expressed as pH value rather than amount of gastric H(+) secreted per unit time. Gastric acid secretion is regulated by endocrine, paracrine and neurocrine signals via at least three messenger pathways: gastrin-histamine, CCK-somatostatin, and neural network. These pathways have been largely validated and further characterized by phenotyping a series of knockout mouse models. The complexity of gastric acid secretion is illustrated by both expected and unexpected phenotypes of altered acid secretion. For examples, in comparison with wild-type mice, gastrin and CCK double knockout and SSTR(2) knockout mice displayed a shift in the regulation of ECL cells from somatostatin-SSTR(2) pathway to galanin-Gal1 receptor pathway; a shift in the regulation of parietal cells from gastrin-histamine pathway to vagal pathway; and a shift in the CCK(2) receptors on parietal cells from functional silence to activation. The biological function of glycine-extended gastrin in synergizing gastrin-17 has been revealed in gastrin knockout mice. The roles of gastric acid secretion in tumorigenesis and ulceration have not been fully understood. Transgenic hypergastrinemic INS-GAS mice developed a spontaneous gastric cancer, which was associated with an impaired acid secretion. Gastrin knockout mice were still able to produce acid in response to vagal stimulation, especially after H. pylori infection. Taken together, phenotyping of a series of genetically engineered mouse models reveals a high degree of complexity of gastric acid secretion in both physiological and pathophysiological conditions.

Topics: Animals; Cholecystokinin; Gastric Acid; Gastrins; Gene Targeting; Helicobacter Infections; Helicobacter pylori; Humans; Mice; Mice, Knockout; Paracrine Communication; Peptic Ulcer; Receptors, Somatostatin; Stomach Neoplasms

The purpose of this paper is to investigate the relationship between clinical outcome and the intactness of cagPAI in Helicobacter pylori strains from Vietnam. The presence or absence of 30 cagPAI genes was investigated by polymerase chain reaction (PCR) and dot-blotting. H. pylori-induced interleukin-8 secretion and hummingbird phenotype, and H. pylori adhesion to gastric epithelial cells were examined. The serum concentration of pepsinogen 1, pepsinogen 2, and gastrin was also measured in all patients. cagPAI was present in all 103 Vietnamese H. pylori isolates, of which 91 had intact cagPAI and 12 contained only a part of cagPAI. Infection with the partial cagPAI strains was less likely to be associated with peptic ulcer and chronic gastric mucosal inflammation than infection with strains possessing intact cagPAI. The partial cagPAI strains lacked almost all ability to induce interleukin-8 secretion and the hummingbird phenotype in gastric cells. Their adhesion to epithelial cells was significantly decreased in comparison with intact cagPAI strains. Moreover, for the first time, we found an association between cagPAI status and the serum concentration of pepsinogens 1 and 2 in infected patients. H. pylori strains with internal deletion within cagPAI are less virulent and, thus, less likely to be associated with severe clinical outcomes.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Bacterial Adhesion; Bacterial Proteins; DNA, Bacterial; Epithelial Cells; Female; Gastrins; Genomic Islands; Helicobacter Infections; Helicobacter pylori; Humans; Interleukin-8; Male; Middle Aged; Pepsinogen A; Peptic Ulcer; Polymerase Chain Reaction; Polymorphism, Genetic; Vietnam; Virulence; Virulence Factors; Young Adult

To study the value of serum biomarker tests to differentiate between patients with healthy or diseased stomach mucosa: i.e. those with Helicobacter pylori (H pylori) gastritis or atrophic gastritis, who have a high risk of gastric cancer or peptic ulcer diseases.. Among 162 Japanese outpatients, pepsinogen I (Pg I) and II (Pg II) were measured using a conventional Japanese technique, and the European GastroPanel examination (Pg I and Pg II, gastrin-17 and H pylori antibodies). Gastroscopy with gastric biopsies was performed to classify the patients into those with healthy stomach mucosa, H pylori non-atrophic gastritis or atrophic gastritis.. Pg I and Pg II assays with the GastroPanel and the Japanese method showed a highly significant correlation. For methodological reasons, however, serum Pg I, but not Pg II, was twice as high with the GastroPanel test as with the Japanese test. The biomarker assays revealed that 5% of subjects had advanced atrophic corpus gastritis which was also verified by endoscopic biopsies. GastroPanel examination revealed an additional seven patients who had either advanced atrophic gastritis limited to the antrum or antrum-predominant H pylori gastritis. When compared to the endoscopic biopsy findings, the GastroPanel examination classified the patients into groups with "healthy" or "diseased" stomach mucosa with 94% accuracy, 95% sensitivity and 93% specificity.. Serum biomarker tests can be used to differentiate between subjects with healthy and diseased gastric mucosa with high accuracy.

Topics: Adult; Aged; Biopsy; Diagnosis, Differential; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Japan; Middle Aged; Outpatients; Pepsinogen A; Pepsinogen C; Peptic Ulcer; Prevalence; Reference Values; Risk Factors; Stomach; Stomach Neoplasms; Young Adult

To investigate whether interdigestive gastric acid secretion can be controlled by a possible memory-related cortical mechanism.. To evaluate gastric secretion in rats, we used a methodology that allows gastric juice collection in rats in their habitual conditions (without any restraining) by pairing sound as the conditioning stimulus (CS) and food as the unconditioning stimulus (US). The levels of gastric acid secretion under basal conditions and under sound stimulation were recorded and the circulating gastrin levels determined.. When the gastric juice was collected in the course of the conditioning procedure, the results showed that under noise stimulation a significant increase in gastric acid secretion occurred after 10 days of conditioning (p<0.01). The significance was definitively demonstrated after 13 days of conditioning (p<0.001). Basal secretions of the conditioned rats reached a significant level after 16 days of conditioning. The levels of noise-stimulated gastric acid secretion were the highest so far described in physiological experiments carried out in rats and there were no significant increases in the circulating gastrin levels.. The results point to the important role played by cortical structures in the control of interdigestive gastric acid secretion in rats. If this mechanism is also present in humans, it may be involved in diseases caused by inappropriate gastric acid secretion during the interprandial periods.

Topics: Animals; Conditioning, Psychological; Gastric Acid; Gastrins; Male; Peptic Ulcer; Rats; Rats, Wistar

Our aim was to determine the frequency of peptic ulcer and Helicobacter pylori infection by gastrointestinal evaluations in pretransplantation phase in children with end-stage renal disease (ESRD).. Twenty-four children with ESRD (13 girls and 11 boys) with a mean age of 14.7 +/- 3.4 years on maintenance hemodialysis were included in this study. Upper gastrointestinal endoscopies were performed and 4 gastric, antral, and duodenal biopsy specimens were obtained for urease test and histological study. Serum gastrin levels were measured in all patients, too. A control group was chosen to compare the rate of H pylori infection between children with ESRD and healthy children.. Gastrointestinal symptoms were present in 16 (66.7%) of 24 patients. Seventeen (70.8%) patients had abnormal upper gastrointestinal endoscopic findings. Infection with Helicobacter pylori was detected in 16 patients and 5 healthy children (66.7% versus 20.0%, P < .001). The frequency of dyspeptic symptoms was not different significantly between uremic patients with and without H pylori infection (P = .67). The same results were found regarding the upper gastrointestinal abnormalities found by endoscopy (P = .65). Oral alkalizing supplement was received by 63% of symptomatic and 80% of asymptomatic patients. Serum gastrin levels were significantly higher in infected patients than in noninfected patients with H pylori (P < .001).. We found a significant number of patients with peptic ulcer diseases, H pylori infection, and secondary hypergastrinemia. This study showed that clinical symptoms are not a reliable predictor of gastrointestinal problems and this is more confusing in patients who received alkalizing solutions.

Topics: Adolescent; Biopsy; Case-Control Studies; Child; Dyspepsia; Endoscopy, Gastrointestinal; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Kidney Failure, Chronic; Male; Peptic Ulcer; Renal Dialysis; Young Adult

The aim of the present study is to investigate the antiulcerogenic effects of the essential oil (EO) of Croton cajucara Benth in rats fed with a normal protein (NP) and low-protein diet (MN). NP and MN rats were treated with the essential oil for 15 days after chronic ulceration was induced. The EO accelerated healing of acetic acid-induced gastric lesions in NP and MN rats (p<0.05). In a similar experiment on chronic ulceration, Epidermal Growth Factor (EGF) mRNA expression increased in NP rats but not in MN rats. In assays of acute antiulcerogenic activity, C. cajucara increased somatostatin plasma levels and decreased gastrin plasma levels in both animal groups. The EO significantly prevented ethanol-induced gastric ulcers in NP and MN rats (p<0.001). Histological examination showed initial regeneration, formation of inflammatory infiltrate and angiogenesis in the epithelium surface of acetic acid-induced ulcers in NP and MN rats. C. cajucara prevented gastric lesions in both animal groups when ethanol methodology was used. We concluded that the EO showed an antiulcerogenic activity mediated by increased somatostatin secretion and EGF mRNA expression.

Topics: Acetic Acid; Animals; Anti-Ulcer Agents; Base Sequence; Croton; Dietary Proteins; DNA Primers; Epidermal Growth Factor; Female; Gastrins; Malnutrition; Peptic Ulcer; Rats; Rats, Wistar; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Somatostatin

Gastrointestinal tract (GIT) is the most common organ system involved in systemic sclerosis (SSc). GIT involvement is mainly attributed to GIT dismobility and wide mouth diverticular. GIT involvement in SSc can be also severely debilitating and even life threatening. To our knowledge, the presence of gastrointestinal bleeding due to the presence of multiple peptic ulcers in scleroderma patients is not well described. In this case report, we describe a scleroderma patient with recurrent gastrointestinal bleeding due to multiple peptic ulcers, in which vagotomy, pyloroplasty, and cholocystectomy were performed and subcutaneous somatostatin was administered to discontinue the recurrent bleeding and stabilize her clinical condition.

Topics: Female; Gastrins; Hormones; Humans; Injections, Subcutaneous; Middle Aged; Peptic Ulcer; Peptic Ulcer Hemorrhage; Scleroderma, Systemic; Somatostatin

The Zollinger-Ellison syndrome is characterized pathophysiologically by a significant hypergastrinemia derived from a gastrin-secreting neuroendocrine tumor with a primary location in the pancreas or duodenum. Chronic hypergastrinemia in turn triggers gastric acid hypersecretion yielding in chronic or recurrent or refractory peptic ulcer disease and/or chronic diarrhea. One half of patients with ZES will have distant metastases in the liver by the time the diagnosis is established and one half of all patients with ZES will experience chronic diarrhea as chief complaint rather than peptic ulcer-related symptoms and signs. Gastrinomas have been reported to either manifest sporadically or to occur in conjunction with the genetic background of the MEN-I syndrome. Diagnosis is based on the patients history which is typically characterized by recurrent episodes of peptic ulcer disease or by severe reflux esophagitis and/or diarrhea or by acid-related symptoms which fail to respond to standard treatment regimens. Upper gastrointestinal tract endoscopy will provide evidence for peptic ulcer disease in anatomical regions located aborally the duodenal bulb within the descending part of the duodenum or even farther distally within the jejunum. Peptic ulcers frequently occur in groups indicating some substantial acid hypersecretion. A gastric pH > 2 is mutually exclusive for ZES. Increased serum gastrin levels confirm the diagnosis biochemically. Gastrin secretion can be determined in the basal state or following stimulation with secretin or calcium. High sensitivity and specificity for the diagnosis of ZES is provided by determining the ratio of basal versus pentagastrin-stimulated gastric acid secretion: The ratio of BAO / MAO > 0.6 is highly specific for gastrinoma. To localize the gastrin-secreting tumor computer-assisted tomography, endoscopic ultrasound, and somatostatin receptor scintigraphy provide useful help but most recently, endoscopic ultrasound with high resolution transducers appear to improve preoperative site localization. If modern imaging techniques fail to elucidate the site of the tumor, intraoperative diaphany may help to detect gastrinomas within the duodenal wall. Definitive treatment will only be achieved by total surgical resection of the gastrin-producing tumor in the pancreas or duodenum including dissection of the regional lymph nodes. Control of symptoms will have to be achieved by administration of highly potent proton pump inhibitors i

Topics: Diagnosis, Differential; Duodenal Neoplasms; Esophagitis, Peptic; Gastric Acidity Determination; Gastrinoma; Gastrins; Humans; Pancreatic Neoplasms; Peptic Ulcer; Proton Pump Inhibitors; Zollinger-Ellison Syndrome

The aim was to examine the influence of different modalities of peptic ulcer surgery on the gastric emptying (GE) pattern and related serum level changes of selected gut hormones.. Fifty eight subjects were examined. In 48 of them peptic ulcer surgery was performed at least six months before the examination: Billroth I (B1) in 11, Billroth II (B2) in 16, B1 with the selective vagotomy--Harkins 1 (H1) in 9 and B2 with the selective vagotomy--Harkins 2 (H2) in 12. Ten healthy volunteers (C) were also examined.. The results of gastric emptying showed that the lag phase duration was inversely related to the GE rates, and the GE pattern was linear in both controls (C) and in operated patients, except in B2 group, in which the GE pattern was exponential. In comparison with C group, GE was slower in B1, H1 and H2 groups, and faster in B2 group. The plasma gastrin values in C group, showing two peaks, were higher in relation to other groups. In relation to C group, higher values of motilin were obtained in patients after the selective vagotomy. The plasma somatostatin values recorded in B1 and H1 groups, showing the marked peaks, were higher in relation to C group. In relation to C group the highest plasma neurotensin values were obtained in B2 group.. In order to understand entirely the influence of peptic ulcer surgery on the GI function, further research of the role of specific hormones and neuropeptides is needed, which would enable more precise selection of the therapy in order to prevent postvagotomy and postgastrectomy syndromes.

Topics: Gastric Emptying; Gastrins; Gastrointestinal Hormones; Humans; Neurotensin; Peptic Ulcer; Radioimmunoassay; Time Factors; Vagotomy

For treatment of giant perforated peptic ulcers, we hypothesized that partitioning of the gastric body instead of the antrum would prevent hypergastrinemia and minimize ulcerogenic risk. By maintaining part of the acid-secreting gastric body in continuity with the excluded distal stomach, gastrin-secreting cells in the antrum would still be inhibited by gastric acid secretion from the gastric body.. We studied (1) gastric body partition with gastrojejunostomy in 8 critically ill patients with giant perforated peptic ulcers and (2) the influence of gastric partition on serum gastrin in 18 dogs with gastric antral partition + gastrojejunostomy, or gastric body partition + gastrojejunostomy, or gastrotomy.. No patient developed major postoperative complications. Serum gastrin levels were normal in 6 patients but showed an abnormal increase in 2 patients 1 month after gastric body partition. Serum gastrin levels had returned to the normal range at postoperative follow-up after 2 years. In the animal study, serum gastrin levels and the number of G-cells in the excluded antrum and acid-secreting parietal cells in the gastric body were increased when evaluated on day 60 postoperatively or after antral partition, compared with preoperative data in the same group. These changes did not occur in the group undergoing partition of the gastric body and the group undergoing gastrostomy. Postoperative serum gastrin levels, and the number of G-cells and parietal cells also was significantly greater in the antral partition group than in the other 2 groups. No ulcer was found in any dog in the gastric body partition and gastrostomy groups, but ulcers occurred in 4 dogs in the antral partition group, all of whom died of ulcer perforation.. Gastric body partition + gastrojejunostomy is a simple, dependable procedure for patients with perforated giant peptic ulcers. This procedure does not require extreme expertise and can be performed in a very short time, even by a trainee general surgeon in emergency.

Topics: Adult; Aged; Animals; Digestive System Surgical Procedures; Dogs; Gastrins; Humans; Models, Animal; Peptic Ulcer; Peptic Ulcer Perforation; Postoperative Complications; Radiography; Recurrence; Risk Factors

Peptic ulcers due to nonsteroidal anti-inflammatory drug (NSAID) use may have contributed to the static prevalence of ulcer disease in Asia.. We aimed to determine the current etiology of peptic ulcer disease in Singapore.. Consecutive patients undergoing esophagogastroduodenoscopy who had not been exposed to antibiotics, or antiulcer therapy within the past 6 months, and in whom peptic ulcers were found, were prospectively studied. Before endoscopy, patients were interviewed regarding the use of NSAID or aspirin. During endoscopy, antral biopsies were obtained for urease test and histology. Serum thromboxane B2 levels were compared with those of healthy volunteers.. Peptic ulcers were detected in 600 patients during a 2-year period. The ulcers were negative for Helicobacter pylori in 212 patients (35.3%) and these H. pylori negative ulcers were related to NSAID use in 68.9% of cases. On the basis of serum thromboxane B2 levels, 30.8% of the patients with non-H. pylori non-NSAID were considered to have consumed NSAID.. H. pylori negative peptic ulcer makes up a significant proportion of peptic ulcer in Singapore. Most of these ulcers were related to NSAID use. Serum thromboxane profile suggested surreptitious NSAID use in many of the non-H. pylori and apparently non-NSAID patients.

Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Female; Gastrins; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Peptic Ulcer; Prospective Studies; Singapore; Thromboxane B2

This is our final report on the clinical effectiveness and safety of long-term pantoprazole in patients with severe peptic ulcer or reflux disease during continuous treatment for up to 5 years.. Patients (n= 150) with peptic ulcer or reflux erosive oesophagitis running an aggressive course or with complications, and refractory to H2-receptor antagonists, were entered into this 5-year programme. Assessment was by serial endoscopy, clinical examination, serum gastrin estimation, gastric mucosal histology and mucosal endocrine cell quantification.. Healing results were presented earlier. The estimated rates of remission on maintenance treatment with pantoprazole (n = 115) were 82% at 1 year, 75% at 2 years, 72% at 3 years, 70% at 4 years and 68% at 5 years. Helicobacter pylori infection appeared not to influence the outcome in reflux patients, with roughly two-thirds continuing in remission irrespective of infection. Only four patients had adverse events considered to be definitely related to pantoprazole. Median gastrin levels rose by 1.5-2-fold and were higher in those with H. pylori infection; 13 patients had levels >500 ng/L on at least one occasion, but these high levels were not sustained. Histological changes were more marked in patients infected with H. pylori: chronic gastritis decreased in the antrum and increased in the corpus, which also showed atrophic changes. The total number of endocrine cells in the antrum showed little variation over 60 months but fell by around one-third in the corpus.. Long-term treatment with pantoprazole is effective and safe.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adult; Aged; Anti-Ulcer Agents; Benzimidazoles; Cell Count; Enteroendocrine Cells; Female; Gastric Mucosa; Gastrin-Secreting Cells; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Pantoprazole; Peptic Ulcer; Sulfoxides

In 1905, John Edkins (1863-1940) undertook the studies of gastrin that have subsequently formed the basis for a century of investigation into the physiological basis of acid secretion and led to the elucidation of a variety of acid-suppressive pharmacological agents that have revolutionized the management of acid peptic disease. Although his name is known to few, his contributions to the physiology of gastric secretion and his study of spiral organisms in the stomach were prescient and to this day remain models of insightful and rigorous research. As a mentor, his educational impact was exemplified by the fact that he was the first to teach physiology to women in the United Kingdom. Gastrin has evolved from an initially unaccepted phenomenon, to be recognized as an important hormone and a fundamental component of regulatory biology as well as a clinically relevant biomarker of disease. Its critical role in the modulation of acid secretion has become a sine qua non and has been extended to include a broad regulatory proliferative role in the mucosa of the gastrointestinal tract. The pivotal role of gastrin in gastric physiology, biology and clinical medicine is now well accepted and reflects the fundamental contributions that Edkins made to the identification of the agent and the elucidation of its function. As a result of the delineation of the neural and hormonal regulatory mechanisms of acid secretion, the scientific basis of acid peptic disease has become apparent. The identification of histamine receptors and proton pumps has led to the discovery of novel pharmacotherapeutic agents capable of producing acid suppression of such efficacy that surgery has become virtually obsolete in the treatment of the disease process. A century after the initial observations by Edkins of gastrin, the identification of Helicobacter pylori and the ability to eradicate it, as well as the use of the proton pump inhibitor class of drugs, have revolutionized the management of gastroduodenal ulceration and gastroesophageal reflux disease. Both patients and physicians owe a great debt to Edkins, whose seminal observations regarding gastrin initiated an era of gastrointestinal scientific, clinical and pharmacological advance that has culminated in the ability to treat and cure acid peptic disease.

Topics: Animals; Anti-Ulcer Agents; England; Gastric Acid; Gastrins; Gastrointestinal Tract; History, 20th Century; Humans; Peptic Ulcer

Recently we have reported synergistic effects between glycine-extended gastrin (G-gly) and amidated gastrin-17 on acid secretion in short-term infusion studies. In the present study, we examined the long-term effect of G-gly on the atrophy-promoting effects of amidated gastrin in the mouse stomach with or without Helicobacter infection. Transgenic mice overexpressing amidated gastrin (INS-GAS mice), G-gly (MTI/G-gly mice), and both peptides (INS-GAS/G-gly mice) were used for assessment of acid secretion and ulcer susceptibility and histologic examination and scoring of preneoplastic lesions in response to the 3 and 6 months Helicobacter felis (H. felis) infection. We found that MTI/G-gly mice had normal gastric histology and acid secretion. Double transgenic (INS-GAS/G-gly) mice showed 2-fold increases in acid secretion compared with INS-GAS mice. Acute peptic ulcers after pyloric ligation were noted in 50% of the INS-GAS/G-gly mice but in none of the INS-GAS mice at 6 months of age. Whereas male INS-GAS mice had a >50% decrease in the numbers of parietal cell and enterochromaffin-like cell at 6 months of age, the male double transgenic mice had no such decrease. Overexpression of G-gly reduced the scores of preneoplasia in the stomach; however, it did not prevent the development of amidated gastrin-dependent gastric cancer in both H. felis-infected mice and uninfected mice. We conclude that G-gly synergizes with amidated gastrin to stimulate acid secretion and inhibits parietal cell loss in INS-GAS/G-gly mice. The overexpression of G-gly seems to increase the susceptibility to peptic ulcer disease and delay the development of Helicobacter-mediated gastric preneoplasia in this model.

Topics: Animals; Disease Susceptibility; Gastrins; Glycine; Mice; Mice, Transgenic; Parietal Cells, Gastric; Peptic Ulcer; Stomach

In Japan, most cases of gastric carcinoid tumor (GCT) are unassociated with either autoimmune gastritis (AIG) showing type-A chronic atrophic gastritis (CAG-A) or Zollinger-Ellison syndrome (ZES). However, the pathogenesis of this tumor remains unknown. Recent studies have determined that Helicobacter pylori infection induces gastric carcinoid in Mongolian gerbils and that H. pylori lipopolysaccharide exerts a mitogenic effect on ECL cells. We examined five patients with histologically diagnosed GCT, 40 patients with H. pylori-positive gastric ulcer (Hp+GU), 24 patients with H. pylori-positive duodenal ulcer (Hp+DU), and 12 patients with AIG showing CAG-A topographically. We compared the prevalence of H. pylori infection, and the levels of gastrin and pepsinogen (PG) in the serum of patients with GCT with those of patients with Hp+GU, or Hp+DU, and AIG. We also investigated the histological characteristics of the tumor and the gastric corpus mucosa in the GCT patients. The levels of serum gastrin and PG I and II were measured using an RIA kit. In all five (100%) patients with GCT, H. pylori infection was present, without any evidence of AIG or ZES. The serum levels of gastrin in the GCT patients were higher than those in either Hp+GU or Hp+DU patients and lower than those in the AIG patients. In contrast, serum PG I levels and the PG I/II ratio were lower in the GCT group than in the Hp+GU or Hp+DU groups. Histologically, all GCTs were ECL cell tumors and peritumoral corporal mucosal atrophy was observed in four of the five patients with GCT. In conclusions, H. pylori infection and hypergastrinemia were found in the patients with GCT without AIG. This finding suggests that H. pylori infection may induce corporal mucosal atrophy and hypergastrinemia that can produce a GCT with time.

Topics: Adult; Aged; Aged, 80 and over; Autoimmune Diseases; Carcinoid Tumor; Duodenal Ulcer; Female; Gastrins; Gastritis; Gastritis, Atrophic; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Pepsinogen C; Peptic Ulcer; Stomach Neoplasms

We describe herein the case of a 54-year-old Japanese woman in whom an inveterate peptic ulcer developed in association with pseudo-Zollinger-Ellison Syndrome (pseudo-ZES). The patient presented with weight loss and abdominal distension caused by antral and duodenal stenosis due to an inveterate peptic ulcer. Her serum gastrin level was very high; however, no evidence of a gastrinoma or carcinoid tumor was detected by preoperative examinations or surgery. A total gastrectomy and double-tract reconstruction was performed, and pathological examination revealed a gastric ulcer (UL-IV) with no histopathological evidence of a neoplasm. Immunohistochemical staining showed an obvious increase in the number of endocrine cells that were positive for chromogranin A, and marked G-cell hyperplasia was observed in the antral mucosa. Furthermore, the number of enterochromaffin-like cells was remarkably high. From the results of the immunohistochemical examination, the patient was diagnosed as having hypergastrinemia due to antral G-cell hyperplasia. Postoperatively, the patient's serum gastrin level fell rapidly to within the normal range, her nutritional status improved, and her weight increased by about 10 kg within 1 year.

Topics: Diagnosis, Differential; Female; Gastrectomy; Gastrin-Secreting Cells; Gastrinoma; Gastrins; Humans; Hyperplasia; Immunohistochemistry; Middle Aged; Peptic Ulcer; Pyloric Antrum; Treatment Outcome; Zollinger-Ellison Syndrome

The polymorphic enzyme CYP2C19 is of importance for the metabolism and effects of omeprazole during short-term treatment.. To investigate the relationship between CYP2C19 genotype and the effects of long-term omeprazole treatment.. A total of 180 patients with acid related disorders were genotyped for wild type and mutated CYP2C19 alleles by allele-specific PCR amplification. Gastrin and chromogranin A were assessed by radioimmunoassays, and pepsinogen I and H. pylori serology were assessed by ELISA methods.. In 108 of the patients, who received a single dose of 20 mg omeprazole, there was no difference in gastrin and chromogranin A concentrations between the three CYP2C19 genotypes. In 72 patients on long-term treatment (> 1 year) with 20 mg omeprazole daily, serum gastrin as well as plasma chromogranin A concentrations (mean +/- s.e.) were both about threefold higher in the wild type/mutated (52.1 +/- 7.6 pM and 7.3 +/- 1.3 nM (n=19), respectively) compared to wild type/wild type (14. 7 +/- 0.9 pM and 2.5 +/- 0.1 nM (n=52), respectively; both comparisons P=0.0001). In a single mutated/mutated patient on long-term treatment, both gastrin and chromogranin A were high (88 pM and 13.7 nM, respectively). Serum pepsinogen I concentration was significantly lower in wild type/mutated (n=19) patients on long-term treatment, compared with the corresponding wild type/wild type (n=49) group (147 +/- 19 microg/L vs. 193 +/- 12 microg/L, P=0. 04).. Patients with one (and probably also with two) mutated CYP2C19 allele(s) on long-term treatment with omeprazole had significantly affected serum gastrin and pepsinogen I and plasma chromogranin A concentrations compared with patients with two normal alleles. This indicates that changes in gastric mucosal morphology during omeprazole treatment might be dependent upon the degree of the individual's capacity to metabolize omeprazole.

Topics: Anti-Ulcer Agents; Aryl Hydrocarbon Hydroxylases; Biomarkers, Tumor; Chromogranin A; Chromogranins; Cytochrome P-450 CYP2C19; Cytochrome P-450 Enzyme System; Enzyme-Linked Immunosorbent Assay; Female; Gastric Mucosa; Gastrins; Gastroesophageal Reflux; Genotype; Helicobacter pylori; Humans; Male; Middle Aged; Mixed Function Oxygenases; Omeprazole; Pepsinogen A; Peptic Ulcer; Polymorphism, Genetic; Radioimmunoassay

Ulcer healing involves expression of various growth factors including hepatocyte growth factor (HGF) at the ulcer margin and the rise in plasma gastrin but the effects of locally applied HGF and gastrin, which are known to act as trophic factors for the gastric mucosa, with or without neutralizing antibodies against HGF and gastrin or COX-1 and COX-2 inhibitors on ulcer healing and the expression of cyclooxygenase (COX)-1 and COX-2 during this healing have been little studied. Rats with gastric ulcers induced by serosal application of acetic acid (ulcer area 28 mm2) received a submucosal injection of either: 1)vehicle (saline), 2) HGF and 3) gastrin with or without neutralizing antibodies against HGF and gastrin or treatment with indomethacin (2 mg/kg-d i.p.), a non-specific inhibitor of COX, or NS-398 (5 mg/kg-d i.g.) and Vioxx (10 mg/kg-d i.g.), both highly specific COX-2 inhibitors. Each growth factor and specific antibodies against HGF and gastrin (100 ng/100 microl each) were injected just around the ulcer immediately after ulcer induction and this local application was repeated at day 2 following anesthesia and laparotomy. At day 13 and 21, the area of ulcers was determined by planimetry, the gastric blood flow (GBF) at ulcer margin was examined by H2-gas clearance technique and mucosal generation of PGE2 and the expression of COX-1 and COX-2 mRNA in the non-ulcerated and ulcerated gastric mucosa was analyzed using RT-PCR. The gastric ulcers healed progressively within 21 days and this effect was accompanied by significant increase in the GBF at the ulcer margin and expression of COX-2 mRNA and COX-2 protein at the ulcer area. Treatment with HGF and gastrin significantly accelerated the rate of ulcer healing and raised GBF at ulcer margin causing further significant upregulation of COX-2 mRNA and COX-2 protein (but not of COX-1 mRNA ) in the ulcerated mucosa. The upregulation of COX-2 mRNA induced by HGF was significantly attenuated by the concurrent local treatment with antibody against this growth peptide. Indomethacin and both COX-2 inhibitors significantly prolonged the ulcer healing, while suppressing the generation of PGE2 in non-ulcerated and ulcerated gastric mucosa and the GBF at ulcer margin. The acceleration of ulcer healing by HGF and gastrin and accompanying rise in the GBF at ulcer margin were significantly attenuated by the concurrent treatment with indomethacin or NS-398 and Vioxx. HGF injections produced a significant rise in the pl

Topics: Animals; Antibodies; Blotting, Western; Cyclooxygenase 1; Cyclooxygenase 2; Cyclooxygenase 2 Inhibitors; Cyclooxygenase Inhibitors; Dinoprostone; Enzyme Inhibitors; Gastric Mucosa; Gastrins; Hepatocyte Growth Factor; Indomethacin; Isoenzymes; Lactones; Male; Membrane Proteins; Nitrobenzenes; Peptic Ulcer; Prostaglandin-Endoperoxide Synthases; Rats; Rats, Wistar; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Sulfonamides; Sulfones

The effects of Helicobacter pylori infection on gastric acid secretion has not been clarified. The aim of this study was to elucidate the effects of H. pylori infection on gastric juice pH in relation to gene expression of interleukin-1beta (IL-1beta), which is reported to inhibit gastric acid secretion. Gastric juice pH and serum gastrin levels were measured in patients with peptic ulcer disease. The amount of IL-1beta mRNA in gastric fundic gland mucosa was also measured by a competitive reverse transcription-polymerase chain reaction method. These parameters were determined before and after treatment with lansoprazole and amoxicillin. Before treatment a significant positive relation was observed between the amount of IL-1beta mRNA in gastric fundic gland mucosa and gastric juice pH. After treatment significant decreases in the amount of IL-1beta mRNA, gastric juice pH, and serum gastrin levels were observed in patients with eradication of H. pylori, whereas no significant changes were observed in patients without eradication. These results suggest that H. pylori infection induces IL-1beta and suppresses acid secretion, resulting in increases in gastric juice pH and serum gastrin levels. Eradication of H. pylori decreases IL-1beta induction, resulting in an increase in gastric juice acidity and normalization of serum gastrin levels.

Topics: Base Sequence; DNA, Complementary; Duodenal Ulcer; Female; Gastric Acid; Gastric Juice; Gastric Mucosa; Gastrins; Gene Expression Regulation; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Interleukin-1; Male; Middle Aged; Molecular Sequence Data; Peptic Ulcer; Reverse Transcriptase Polymerase Chain Reaction; RNA, Messenger; Severity of Illness Index; Stomach Ulcer

Topics: Anti-Ulcer Agents; Cysts; Female; Gastric Mucosa; Gastrins; Gastrointestinal Hemorrhage; Gastrostomy; Humans; Infant; Jejunostomy; Peptic Ulcer; Pyloric Antrum; Ranitidine; Stomach Diseases; Vagotomy

This study evaluates whether a new analytic principle, processing-independent analysis (PIA), offers better specificity and sensitivity than the conventional gastrin radioimmunoassay in the diagnosis of gastrinomas.. Plasma concentrations of alpha-amidated gastrins and the total progastrin product were measured with radioimmunoassay and with PIA, respectively, in 512 samples taken for gastrin measurement and in a selected group of gastrinoma patients (n=10).. Among the 512 patients were 9 with gastrinomas. In plasma from these patients the median degree of amidation (ratio of alpha-amidated gastrins to total progastrin product) was 75% (range, 25-98%), whereas in the other groups the medians varied from 41% to 86%. In the second group of gastrinoma patients all had a degree of amidation of less than 50%.. In screening for gastrinomas PIA offered no diagnostic advantages in comparison with conventional gastrin radioimmunoassay. However, in selected patients who in spite of normal or slightly increased concentrations of amidated gastrins were still suspected of having gastrinoma, additional measurement of the total progastrin product showed incomplete processing of progastrin and thus proved helpful in establishing the diagnosis.

Topics: Anti-Ulcer Agents; Case-Control Studies; Female; Gastrinoma; Gastrins; Humans; Male; Middle Aged; Pancreatic Neoplasms; Peptic Ulcer; Protein Precursors; Radioimmunoassay; Sensitivity and Specificity; Zollinger-Ellison Syndrome

In order to explore the role of Helicobacter pylori (H. pylori) infection in hypergastrinemia in patients on dialysis, the changes in serum gastrin concentration were examined before and after eradication treatment for H. pylori. Twenty-seven patients on dialysis were treated for the eradication of H. pylori. Fasting serum gastrin concentrations were measured by a radioimmunoassay which detects gastrin 17. Ammonia and pH levels of the gastric juice were also measured. The serum gastrin concentrations were significantly decreased following eradication of H. pylori, and the mean value reached the normal range. The restoration of hypergastrinemia was associated with marked reductions of gastric juice ammonia and pH levels. In contrast, patients in whom H. pylori was not eradicated showed no changes in these parameters. In conclusion, the elevation of the fasting serum gastrin 17 concentration seen in dialysis patients appeared to be attributable to H. pylori infection in the stomach.

Topics: Ammonia; Anti-Bacterial Agents; Anti-Ulcer Agents; Drug Therapy, Combination; Female; Gastric Juice; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Male; Metronidazole; Middle Aged; Peptic Ulcer; Renal Dialysis

There is strong evidence accumulating that chronic infection with Helicobacter pylori (H. pylori) interferes with inhibitory pathways of the regulation of acid secretion. The increase in maximum acid output (MAO), and the increase in the sensitivity of the parietal cell to gastrin commonly observed in patients suffering from duodenal ulcer disease (DU), however, remains largely unexplained. Insufficient evidence is available concerning how these parameters are influenced by H. pylori infection in patients not suffering from peptic ulcer disease (PUD) and how they are related to H. pylori-induced gastritis. The aim of this study was to compare basal gastric acid secretion (BAO), MAO, and the sensitivity of the parietal cell to gastrin in H. pylori-positive and H. pylori-negative patients not suffering from PUD, and to study the relationship with their individual postprandial gastrin release and the degree of gastric antral and corpus gastritis.. H. pylori status was assessed by CLO test and histology (two biopsies each from the antrum and the corpus) in 14 H. pylori-positive and 16 H. pylori-negative nonulcer patients of comparable age, weight and gender. Gastritis score was assessed by a pathologist, who was unaware of the acid secretory data. Following determination of BAO, the relation of pentagastrin and gastric acid secretion was established with a cumulative pentagastrin dose response curve for the dose range 0.03-6.0 microg/kg(-1) h(-1) and MAO (Vmax) and pentagastrin sensitivity (ED50) were determined. Basal and postprandial gastrin release was measured by radioimmunoassay.. There was a significant higher gastritis score in the H. pylori-positive compared with the H. pylori-negative subjects. The dose response curves of the pentagastrin stimulated gastric acid secretion were not different between H. pylori-positive and H. pylori-negative groups. No correlation was seen between the gastritis score, basal acid output (BAO) peak acid output (PAO), maximum acid output (MAO), ED50 values and the plasma gastrin values. There was, however, a considerable larger variation of the PAO and MAO data of the H. pylori-infected subjects and >50% of the respective data was above or below the relatively low range of the respective values of the noninfected subjects.. H. pylori-induced gastritis does not regularly enhance maximum acid output in nonulcer patients, nor does it modify the sensitivity of the parietal cell to gastrin. H. pylori infection is thus unlikely to be directly responsible for an increase of these parameters in DU disease. Our data support, however, the concept that chronic H. pylori infection can either enhance or attenuate maximum acid secretory capacity in certain subgroups of patients.

Topics: Adult; Biopsy; Dose-Response Relationship, Drug; Female; Gastric Acid; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Linear Models; Male; Middle Aged; Pentagastrin; Peptic Ulcer; Postprandial Period; Statistics, Nonparametric; Stimulation, Chemical

To determine the clinical significance of Helicobacter pylori seropositivity and seronegativity in healthy blood donors, we carried out a serological evaluation of Helicobacter pylori status and endoscopy in a healthy blood donors population. In all, 1010 donors were screened for Helicobacter pylori by IgG ELISA and assessed for pepsinogen I and gastrin levels by RIA; 298 IgG seropositive and 61 seronegative subjects underwent endoscopy with biopsies. Of 359, 165 were also tested for CagA by western blotting. Of the 298 IgG seropositives, 274 were shown to be infected on biopsy testing. Endoscopy revealed 70 peptic ulcers, 41 cases of erosive duodenitis, and two gastric cancers. In all 105 seropositive donors were tested for CagA and 69 were CagA positive [34/58 gastritis (58.6%), 24/35 duodenal ulcer (68.6%) and 11/12 gastric ulcer (91.6%)]. Histologically active/chronic gastritis was associated with CagA: 88.4% vs 50% (CagA seropositive vs seronegative). Of the 61 IgG seronegatives, 59 were negative on biopsy testing. At endoscopy three had duodenitis. Of the 60/61 IgG seronegatives tested for CagA, one had a moderate reaction. Duodenal ulcer donors showed higher pepsinogen I levels than donors without duodenal ulcers (97.7 microg/ml vs 80.9 microg/ml respectively). Screening for Helicobacter pylori and anti-CagA seropositivity and pepsinogen I can identify individuals likely to have gastroduodenal pathology even in the absence of symptoms.

Topics: Adolescent; Adult; Aged; Antibodies, Bacterial; Blood Donors; Blotting, Western; Dyspepsia; Endoscopy, Gastrointestinal; Female; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Pepsinogen A; Peptic Ulcer

Effects of long term administration of Histamine H2-receptor Antagonist (H2-RA) in the treatment of peptic ulcer was studied for the influence to the risk of causing precancerous changes in gastric mucosa. Serum gastrin. ODC activities, polyamine and PCNA labeling index were biochemically and immunohistologically observed. Rat's mucosae with experimentally induced peptic ulcer treated with long term H2-RA, showed no morphological changes but at 30 weeks of H2-RA, had significantly higher value in PCNA labeling index and in polyamine (spermidine) quantity compared to control H2-RA alone and ulcer alone groups. These results suggest that long term administration of H2-RA, even after healing of the ulcer, may cause the gastric mucosa to possess a milieu in favour of precancerous changes, due to the increased proliferative activity of the cells.

Topics: Animals; Gastric Mucosa; Gastrins; Histamine H2 Antagonists; Male; Ornithine Decarboxylase; Peptic Ulcer; Polyamines; Precancerous Conditions; Rats; Rats, Wistar; Stomach Neoplasms; Triazoles

This study was performed to examine the effects of additional enprostil administration on hypergastrinemia and gastric acid suppression induced by omeprazole. Serum gastrin concentrations were measured in 10 peptic ulcer patients (six Helicobacter pylori-positive and four Helicobacter pylori-negative patients) before treatment, after two weeks of omeprazole (20 mg/day), and after two weeks of omeprazole and enprostil (50 micrograms/day). The additional acid inhibitory effect of enprostil was evaluated by 24-hr intragastric pH measurements in five healthy Helicobacter pylori-negative volunteers. After omeprazole treatment, the serum gastrin level of Helicobacter pylori-positive patients (3.5-fold of control) was markedly higher than that of Helicobacter pylori-negative patients (1.7-fold of control). Additional treatment with enprostil suppressed serum gastrin levels to 0.4-fold and 0.7-fold of omeprazole treatment levels in Helicobacter pylori-positive and Helicobacter pylori-negative patients, respectively. In healthy volunteers, median pH recorded during the nonmeal daytime interval increased significantly with additional enprostil. Thus, enprostil reduces undesirable omeprazole-induced hypergastrinemia, especially in Helicobacter pylori-positive patients, and effectively suppresses acid secretion.

Topics: Adult; Aged; Anti-Ulcer Agents; Drug Therapy, Combination; Enprostil; Female; Gastric Acid; Gastric Acidity Determination; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer

The relationship between gastric mucosal damage induced by stress, peptides present in the gastric mucosa and is not clear. Aim of this study was to determine whether cold-restraint stress affected the release of gastric somatostatin, gastrin and in the isolated perfused stomach preparation.. Male Sprague-Dawley rats were used, 12 cold-restraint stressed and 12 unstressed controls. 4 additional unstressed rats were treated with aspirin (100 mg/kg p.o.). After 30 minutes, isolated stomachs were perfused for 50 minutes with Krebs-Ringer buffer added with isoproterenol or carbamylcholine plus somatostatin-14 or carbamylcholine alone, somatostatin, gastrin and prostaglandin E2 release in the portal vein effluent were measured by radioimmuno-assay. Histology of the gastric mucosa was obtained from a further 4 stressed and 4 unstressed rats.. In the stomach from stressed animals, the somatostatin response to isoproterenol and the prostaglandin E2 response to carbamylcholine plus somatostatin were significantly lower than in the controls, whereas gastrin response to carbamylcholine was enhanced by stress. Treatment with aspirin abolished the prostaglandin E2 response to stimulation. Gastric mucosa histology from stressed and unstressed animals showed no significant lesions.. The inhibition of gastric somatostatin and prostaglandins release coupled to an enhanced acid stimulatory influence appear to antidate gastric mucosal injury and should play a role in the stress ulcer genesis.

Topics: Analysis of Variance; Animals; Dinoprostone; Gastric Mucosa; Gastrins; In Vitro Techniques; Male; Peptic Ulcer; Rats; Rats, Sprague-Dawley; Somatostatin; Stomach; Stress, Physiological

To determine whether ferrets naturally infected with Helicobacter mustelae were hypergastrinemic, compared with ferrets that were specific-pathogen-free (SPF) for H mustelae.. Plasma gastrin concentrations in H mustelae-infected and SPF ferrets were measured at 3 time points and compared to determine whether H mustelae was associated with hypergastrinemia.. 21 H mustelae-infected ferrets and 10 SPF ferrets.. The H mustelae status of the ferrets was confirmed prior to commencement of the study. Gastric endoscopy was used to obtain gastric mucosal pinch biopsy specimens that were processed for rapid-urease assay, microaerophilic culturing, and histologic evaluation. Plasma gastrin concentrations were determined at 3 time points: baseline after a 12-hour nonfeeding period, and 30 and 60 minutes after oral administration of a standardized meal. Gastrin was measured by radioimmunoassay.. The results for the H mustelae-infected group (mean +/- SEM pg/ml) were: baseline, 54.4 +/- 2.56; 30 minutes, 94.5 +/- 6.05; and 60 minutes, 82.6 +/- 5.73. The SPF group results were: baseline, 55.8 +/- 7.35; 30 minutes, 80.8 +/- 5.77; and 60 minutes, 59.7 +/- 4.95. There was a significant (P < 0.01) difference at the 60-minute time point between the 2 groups of animals. The H mustelae group had a 17% higher mean gastrin value at 30 minutes.. Helicobacter mustelae is associated with hypergastrinemia in ferrets.. Helicobacter-induced hypergastrinemia may be related to the pathogenesis of peptic ulcer disease in ferrets.

Topics: Animals; Biopsy; Ferrets; Gastric Mucosa; Gastrins; Helicobacter; Helicobacter Infections; Peptic Ulcer; Radioimmunoassay; Specific Pathogen-Free Organisms

Gastric and duodenal biopsies from 90 patients with various acid peptic disorders-reflux esophagitis (n = 24), gastric ulcer (n = 13), duodenal ulcer (n = 47) and nonulcer dyspepsia (n = 6)-were examined. Seven patients with minimal dyspeptic symptoms and an endoscopically and histologically normal stomach and duodenum served as controls. Immunoperoxidase staining for gastrin-producing G cells, somatostatin-producing D cells and serotonin-producing EC cells was carried out on fundic, antral and duodenal biopsies, and was quantified using a Zeiss MOP Videoplan using the peroxidase-antiperoxidase technique of Sternberger. In the gastric antrum, a G:D:EC cell ratio of approximately 1.6:1:1-was observed. In the duodenum the corresponding ratio was 1:1:2.4. No significant differences were observed within any of the major diagnostic categories. Patient age, sex, duration of symptoms, smoking habits, alcohol consumption and nonsteroidal anti-inflammatory drug use had no effect on endocrine cell densities. Reduced G cell density in the descending duodenum was observed in the presence of mild duodenitis in four patients. In four patients with evidence of antral intestinal metaplastic changes, a significant increase in duodenal G cell densities was found. These results suggest that a change in the number of G, D or EC cells does not play a primary role in the pathophysiology of acid peptic disorders in the majority of patients.

Topics: Adult; Aged; Biopsy; Cell Count; Duodenum; Female; Gastric Mucosa; Gastrins; Humans; Immunohistochemistry; Intestinal Mucosa; Male; Middle Aged; Peptic Ulcer; Serotonin; Somatostatin

The risk factors associated with refractory peptic ulcers are still undefined. The purpose of this study was to identify these factors in a multivariate context.. Clinical and endoscopic findings as well as Helicobacter pylori status, gastric secretion analysis, serum gastrin levels, nonsteroidal anti-inflammatory drug (NSAID) use, and objective testing of aspirin use by platelet cyclooxygenase activity were studied in 60 consecutive refractory patients with peptic ulcer and 54 matched nonrefractory controls.. Refractory patients had a longer history of symptomatic ulcer, had an earlier onset, had more frequent relapses, and smoked more during the episode of refractoriness. H. pylori status was similar in both groups, but H. pylori eradication in a subset of refractory patients (23 of 26) was highly effective in healing these ulcers (14 of 23). Globally, NSAID-analgesic abuse (including > 1500 mg/day paracetamol) was present in 40% of refractory patients (P < 0.006). Objective testing showed that 43.7% of NSAID use was surreptitious. Multivariate logistic regression analysis identified only NSAID and analgesic abuse and the number of relapses as individually affecting refractoriness.. NSAID and analgesic abuse is the single most important exogenous factor associated with refractoriness. H. pylori infection emerges as an important intrinsic factor, but almost a quarter of refractory patients cannot be linked to either NSAID use or H. pylori infection.

Topics: Alcohol Drinking; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Blood Platelets; Female; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Peptic Ulcer; Prostaglandin-Endoperoxide Synthases; Regression Analysis; Risk Factors; Smoking; Substance-Related Disorders

To evaluate endogenous and exogenous factors affecting the quality of ulcer healing produced by proton pump inhibitors, gastric acid pH, serum gastrin, and serum pepsinogen (PG) I and II were measured in peptic ulcer patients before and after treatment with lansoprazole 30 mg once daily. Lansoprazole achieved more rapid scarring in duodenal ulcer (n = 34), with a healing rate of 97.1% after 6 weeks, than in gastric ulcer (n = 56), with a healing rate of 92.8% after 8 weeks. Scarring was the most rapid in gastroduodenal ulcer (n = 8), with a healing rate of 100% after 8 weeks, but the rate of complete scarring was the lowest (37.5%). Lower gastric acidity and lower PG I:II ratio were associated with poor quality ulcer scarring in patients with gastric ulcers, but the opposite was true for those with duodenal and gastroduodenal ulcers. For gastric ulcers, not only ulcer size but also mucosal atrophy was an important factor in ulcer healing. Smoking and alcohol consumption had little effect on the quality of ulcer healing during treatment. These results suggest that there are a number of differences between gastric ulcers and duodenal ulcers in terms of the quality of ulcer healing after lansoprazole treatment.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Age Factors; Alcohol Drinking; Anti-Ulcer Agents; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Humans; Lansoprazole; Male; Middle Aged; Omeprazole; Pepsinogens; Peptic Ulcer; Proton Pump Inhibitors; Sex Factors; Smoking; Stomach Ulcer

Gastrin and somatostatin are enterohormones which influence several physiological processes in the gastrointestinal tract. Gastrin has a pro-malignant and pro-ulcerogenic effect, while somatostatin deficiency has a similar effect. The authors examined in their investigation the 24-hour secretion of both hormones in patients with gastric ulcer and atypical gastric conditions. They revealed a significant difference in the 24-hour somatostatin level which was higher in patients with atypical gastric conditions (p < 0.05). The finding may suggest a more intense reaction of somatostatin to malignant than to non-malignant disease. In the other compared parameters no statistically significant difference was revealed.

Topics: Adult; Aged; Female; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Somatostatin; Stomach Diseases

In 66 patients with peptic ulcer (11 with gastric ulcer, 55 with duodenal ulcer, 19 women, 47 men) the serum concentrations of prolactin, dehydrocholic acid and gastrin were determined. The studies were repeated after treatment with ranitidine: in 50 patients after three weeks and in 40 patients after another 30 days. During the first period ranitidine 2 x 150 mg was administered, while during the second period the dose was 1 x 150 mg. The results were compared with those obtained from 120 healthy subjects. Before starting the treatment prolactin levels were significantly higher than those in the control group. During the treatment a significant decrease of the levels was observed. Similar changes of prolactin concentrations were found in the group of 39 men with duodenal ulcer isolated from the studied patients, who were compared with a group of 50 healthy men. It was not found that the development of peptic ulcer and the treatment with ranitidine exerted and effect on the changes of gastrin and dehydrocholic acid concentrations.

Topics: Adult; Anti-Ulcer Agents; Case-Control Studies; Female; Gastrins; Glycocholic Acid; Histamine H2 Antagonists; Humans; Male; Middle Aged; Peptic Ulcer; Prolactin; Ranitidine; Time Factors; Treatment Outcome

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Anti-Ulcer Agents; Blood Chemical Analysis; Combined Modality Therapy; Duodenal Neoplasms; Female; Gastric Acid; Gastric Mucosa; Gastrinoma; Gastrins; Hepatic Artery; Humans; Interferons; Lansoprazole; Male; Middle Aged; Multiple Endocrine Neoplasia; Omeprazole; Pancreatic Neoplasms; Peptic Ulcer; Splenic Artery; Zollinger-Ellison Syndrome

The prevalence of peptic ulcer in cirrhotic patients is similar to that reported for the general population. Although gastric acid outputs ar normal or lower in cirrhotic subjects compared with non-cirrhotics, the frequency of non-response to histamine H2-receptor antagonists is higher. Peptic ulcer disease in the cirrhotic seems to pursue a more virulent course compared with that in the non-cirrhotic subject. Peptic ulcer prevalences in patients dying of uraemia or in uraemic patients on maintenance dialysis treatment are comparable with those in the general population. However, the frequency of peptic ulcer, especially complicated ulcer, is increased following renal transplantation. Ulcer complications in this context are associated with a high mortality rate. Pre-transplant risk factors for subsequent development of peptic ulcer remain to be identified and the value of histamine H2-receptor antagonists in prophylaxis is as yet unproven.

Topics: Duodenitis; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Peptic Ulcer; Peptic Ulcer Hemorrhage; Uremia

Helicobacter pylori infection is associated with increased meal stimulated gastrin secretion, but the reason for this is unknown. Sequence specific radioimmunoassays were used to measure the concentration of alpha-amidated gastrin, the total progastrin product, and somatostatin in biopsy specimens of human antral mucosa. The antral concentrations of alpha-amidated gastrin and of total progastrin products were significantly higher in H pylori infected patients than in those not infected by this organism. In contrast, the antral somatostatin concentration was significantly decreased in infected patients. Progastrin processing, determined by gel chromatography, seemed unaffected by H pylori infection. The results suggest that the finding of increased gastrin secretion from the antral G cells in H pylori infected patients may be a result of reduced inhibition of G-cell secretion by somatostatin.

Topics: Adult; Aged; Aged, 80 and over; Chromatography, Gel; Dyspepsia; Female; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Peptic Ulcer; Protein Precursors; Pyloric Antrum; Radioimmunoassay; Somatostatin

The secretion of hormones stimulating and inhibiting gastric secretory activity was studied in 85 patients with postvagotomy syndromes. The somatropin level was found to increase significantly in gastrostasis. The lower values of the blood insulin and C-peptide content in patients with recurrent ulcers was evidently associated either with insufficiency of the pancreatic insular apparatus or with partial vagal denervation, increased STH level, and plausible inhibiting effect of glucagon. Increased somatostatin secretion in the dumping syndrome, gastrostasis, and peptic ulcers may be due to the encountered hypergastrinemia.

Topics: C-Peptide; Constriction, Pathologic; Diarrhea; Dumping Syndrome; Gastric Acid; Gastrins; Glucagon; Growth Hormone; Humans; Insulin; Insulin Secretion; Neurotransmitter Agents; Peptic Ulcer; Postoperative Complications; Recurrence; Somatostatin; Stomach Diseases; Syndrome; Vagotomy, Proximal Gastric

To study the relationship between Helicobacter pylori infection, gastric inflammatory scores, and fasting gastrin and pepsinogen A and C concentrations, and to evaluate the effect of treatment on these parameters.. Gastrin and pepsinogen A and C concentrations were measured in 36 patients with gastritis, 10 gastric ulcer patients, 12 duodenal ulcer patients, and in 15 subjects with normal gastric mucosa, by standard radioimmunoassay techniques. Fifteen patients with H. pylori infection underwent triple therapy (bismuth subsalicylate, amoxicillin, metronidazole) and were reassessed 1 month later.. Fasting gastrin and pepsinogen A and C concentrations were significantly higher in H. pylori-positive gastritis and peptic ulcer patients than in subjects with normal mucosa and in patients with H. pylori-negative gastritis. There was a significant correlation between inflammatory scores and serum gastrin (r = 0.45, p < 0.0001), and pepsinogen A (r = 0.33, p < 0.006) and pepsinogen C (r = 0.55, p < 0.0001) concentrations. Neither sex nor age affected basal gastrin and pepsinogen concentrations. Eradication of H. pylori infection was successful in 12 patients and resulted in a significant fall in serum gastrin and in pepsinogen A and C concentrations, and in a concomitant improvement of the inflammatory scores. Serum peptide levels and gastritis scores were unchanged in those patients in whom H. pylori infection persisted.. These findings suggest that hypergastrinemia and hyperpepsinogenemia are secondary to H. pylori infection and are related to mucosal inflammation.

Topics: Amoxicillin; Bismuth; Drug Therapy, Combination; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Middle Aged; Organometallic Compounds; Pepsinogens; Peptic Ulcer; Salicylates

The pathogenesis of peptic ulcer is a complex phenomenon and several factors are thought to be involved in this process. Among others, Helicobacter pylori infection, hypergastrinaemia and some proteases seem to play an essential role in inducing peptic ulceration. We investigated whether tryptase (a serine endoprotease released by mast cells) and cathepsin D (a lysosomal hydrolase which seems able to derange the extracellular matrix) play a part in peptic ulcer disease and whether they are linked to Helicobacter pylori infection and mucosal content of gastrin. We studied 13 controls, 25 patients with gastric ulcer, 47 with duodenal ulcer and 11 with duodenitis. Tryptase and cathepsin D were measured in mucosal biopsy specimens (body and antrum of the stomach and duodenum) using IRMA methods. Gastrin was assayed in the antral mucosa by means of a RIA method. Helicobacter pylori infection was histologically evaluated (Giemsa). Tryptase and cathepsin D levels were higher (25%) in patients with active peptic ulcer, whether gastric or duodenal. The mucosal content of cathepsin D, but not that of tryptase, was associated with Helicobacter pylori infection. Tryptase, on the other hand, was related to gastrin content. No correlation was found between the two enzymes. It is concluded that tryptase and cathepsin D probably reflect different pathophysiological modifications in ulcer disease. Cathepsin D seems to be mainly related to the phlogistic reaction of the mucosa to Helicobacter pylori infection; tryptase may reflect and indirect link between the action of gastrin and the function of mast cells.

Topics: Adult; Aged; Cathepsin D; Chymases; Female; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Immunoradiometric Assay; Male; Mast Cells; Middle Aged; Peptic Ulcer; Serine Endopeptidases; Tryptases

Gastric acid is the most important pathophysiologic determinant in the development of peptic ulcer diseases, and gastrin and somatostatin are believed to be physiologic hormonal regulators in gastric acid secretion. The aim of this study is to investigate patterns of these peptides, both in serum and in tissue, and to correlate with numbers of their secretory cells in the antral and the duodenal bulb mucosa.. The study population was made up of 256 patients with peptic ulcer (duodenal ulcer, 127; gastric ulcer, 74) and 55 patients with non-ulcer control subjects. Serum and mucosal concentrations of G17, G34 and somatostatin were measured by radioimmunoassay technique and peptides producing cells were identified immunohistochemically using peroxidase-antiperoxidase staining technique.. Serum G17 concentration was significantly decreased in duodenal ulcer patients (93.4 +/- 36.0 pg/ml) and G34 were more than twice as high as G17 both in patients with gastric and duodenal ulcer (210.6 +/- 50.6 pg/ml and 202.7 +/- 48.1 pg/ml vs 103.8 +/- 41.8 pg/ml and 93.4 +/- 36.0 pg/ml). Antral G17 (19.9 +/- 14.8 mcg/g, tissue) and G34 (26.6 +/- 18.5 mcg/g, tissue) were increased in duodenal ulcer patients and duodenal G17 (12.5 +/- 9.5 mcg/g. tissue in Gu and 8.5 +/- 7.4 mcg/g. tissue in DU) and G34 (15.7 +/- 12.6 mcg/g. tissue in GU and 13.9 +/- 12.0 mcg/g. tissue in DU) concentrations were found to be increased in both gastric and duodenal ulcer patients than in non-ulcer subjects (G17: 5.3 +/- 4.9 mcg/g. tissue. G34: 6.5 +/- 4.4 mcg/g. tissue). Only the antral somatostatin concentration was significantly increased in duodenal ulcer patients (5.3 +/- 5.9 mcg/g. tissue). Numbers of the antral G- and D-cell were lowest in GU patients (48.1 +/- 47.4 and 7.9 +/- 12.3) and numbers of both cells decreased proportionately with the severity of atrophic gastritis and/or intestinal metaplasia of the gastric mucosa. D/G cell ratio between non-ulcer subjects and DU patients was similar (1:4 and 1:5) but slightly increased in GU patients (1:7). There was no correlation between numbers of each peptide-producing cells and serum or mucosal concentration of gastrin and somatostatin.. Patients with duodenal ulcer had decreased level of serum G17 in the fasting state while mucosal concentrations of G17 and G34 were increased in the antrum and the duodenal bulb. Patients with gastric ulcer had increased levels of G17 and G34 only in the duodenal bulb mucosa. Only the antral somatostatin concentration was significantly increased in duodenal ulcer patients. Patients with gastric ulcer had lowest numbers of G- and D-cells in the antrum and numbers of both cells decreased proportionately with the degree of chronic atrophic gastritis and/or intestinal metaplasia of the gastric antrum. Numbers of G- and D-cells were not correlated with the serum or mucosal concentrations of each peptide.

Topics: Adolescent; Adult; Aged; Female; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Somatostatin

The pathomorphological changes in the gastric mucosa and acid production were studied in 118 patients with ulcer disease of a pyloric portion of the stomach and duodenum before and after selective proximal vagotomy in combination with drainage operation. Before the operation, the atrophic changes were the most pronounced in the gastric antrum. Increase in debit of chlorohydric acid was caused by increase in the volume of gastric juice and acid production. Stimulation with food contributes to considerable increase in gastrin concentration in the blood of the patients in low level of glucagon and insulin. Early after the operation, the signs of acute inflammation were revealed in the mucosa of the body and antrum. In increase of a basal level of gastrin and glucagon, acid production significantly decreased. Long-term atrophic gastritis of the body of a stomach was noted mainly in patients with delayed evacuation of its contents. Normalization of the level of hormones correlated with the indices of acid-producing function of the stomach.

Topics: Adolescent; Adult; Female; Gastric Acid; Gastric Juice; Gastric Mucosa; Gastrins; Glucagon; Humans; Male; Middle Aged; Pancreas; Peptic Ulcer; Postoperative Period; Preoperative Care; Pyloric Antrum; Pylorus; Vagotomy, Proximal Gastric

Helicobacter pylori infection is associated with exaggerated gastrin release. We investigated whether this abnormality was due to the bacteria or the immune response. Fasting and meal-stimulated 'total' and amidated gastrin were measured in 10 H. pylori-infected volunteers before eradication therapy, after 2 and 14 days of therapy, and 4 weeks after completion of therapy. The exaggerated meal-stimulated gastrin concentration remained unchanged after 2 days of therapy, although the polymorphonuclear cell infiltrate and H. pylori bacteria were no longer evident. The expected fall in gastrin concentration after 14 days of therapy was associated with a reduction in the density of mucosal mononuclear cells, suggesting exaggerated gastrin release was related to chronic inflammation or to H. pylori or its products. The effect of H. pylori on normal progastrin processing was also assessed; 2 control groups were included: 10 H. pylori-uninfected volunteers and 13 patients with H. pylori peptic ulcers. There was a significant difference in the proportion of circulating gastrins that were biologically active amidated gastrins between ulcer patients and uninfected controls (56.7 +/- 4% versus 33.8 +/- 4%, p < 0.001). The proportion of amidated to total gastrins did not increase after successful eradication.

Topics: Adult; Bismuth; Female; Food; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Male; Metronidazole; Organometallic Compounds; Peptic Ulcer; Protein Precursors; Protein Processing, Post-Translational; Salicylates; Tetracycline

The content of gastrin, pituitary thyrotropin hormone (TTH), the thyroid hormones thyroxin (T4) and triiodothyronine (T3), and 11-OCS in blood serum and the daily catecholamine content in urine were studied in 86 patients in the early periods, 2-4 weeks, after resection of the stomach or selective proximal vagotomy (SPV). The content of gastrin, TTH, T4, and 11-OCS in blood was reduced and catecholamine excretion diminished in patients after gastric resection. After SPV the concentration of gastrin increased and that of TTH reduced. A certain relationship between the clinical course of peptic ulcer and the indices studied was revealed. The application of rehabilitation measures in the early periods after operations on the stomach improves the neuroendocrine regulation in the organism and the functional condition of the alimentary organs.

Topics: 11-Hydroxycorticosteroids; Adult; Catecholamines; Gastrins; Humans; Middle Aged; Peptic Ulcer; Postoperative Period; Thyrotropin; Thyroxine; Time Factors; Triiodothyronine; Vagotomy, Proximal Gastric

Hemodialysis patients are frequently affected by peptic disease, and in many cases they have high serum levels of gastrin. The aim of this study was to evaluate the effects of omeprazole, an inhibitor of gastric parietal cells hydrogen pump, on peptic disease and gastric secretion of 16 selected dialysis patients. H2-receptors blocking drugs or gastric acidity buffers were withdrawn for 2 weeks, then omeprazole was administered for 4 weeks at a daily dosage of 20 mg. Before and after the omeprazole therapy, registration of subjective peptic symptoms, baseline serum gastrin dosage and endoscopy of upper digestive tract were performed. Before starting omeprazole, the serum gastrin value was 515 +/- 180 pg/l, all the patients complained of peptic symptoms, and endoscopy showed: 8 cases of duodenal ulcer, 3 cases of pyloric ulcer and 5 cases of antral erosive gastritis. At the end of the omeprazole treatment period, a slight but statistically not significant increase of serum gastrin level (537 +/- 198 pg/l) was observed. Twelve patients reported the total disappearance of symptoms of peptic disease, 3 patients a partial reduction, and 1 patient had no improvement. Control endoscopy showed the healing (white scar) of all the ulcers, and the disappearance of all the erosive lesions. In conclusion, our results show that a 20 mg/day omeprazole short-term therapy can be given safely to uremic patients undergoing hemodialysis and is effective for a quick healing of active peptic lesions.

Topics: Adult; Drug Administration Schedule; Female; Gastrins; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer; Renal Dialysis; Time Factors; Uremia

The prevalence of Helicobacter pylori (H. pylori) was investigated in 164 consecutive patients with different degrees of renal function; group I (normal renal function) n = 84, group II (chronic renal failure, CLCR > or = 5 < 90 ml/min) n = 45, group III (haemodialysis therapy) n = 35, to test the hypothesis that the resulting different concentrations of urea in the gastric juice would have an influence on the colonization of the gastric mucosa by these urea-splitting bacteria. As every individual method for the detection of H. pylori shows disadvantages, the results of the detection methods used (urease test, Warthin-Starry stain, bacterial cultivation, direct examination of the processed sample by phase-contrast microscopy) were combined in a cumulative evaluation. These calculated cumulative indices for the antrum and corpus showed no statistically significant differences between the studied groups. The prevalence of H. pylori ranged from 34 to 54%. The histopathological findings were similar in all groups. In spite of the fact that patients with renal dysfunction had significantly higher levels of serum gastrin (P < 0.05), there was no influence on the gastric juice pH value. The relationship between the cumulative index and ammonia concentration in gastric juice was found to be linear (P < 0.05). The higher urea levels in the blood and gastric juice of patients with renal failure do not seem to be a risk factor for infection with H. pylori.

Topics: Ammonia; Gastric Juice; Gastric Mucosa; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Hydrogen-Ion Concentration; Kidney Failure, Chronic; Peptic Ulcer; Stomach Ulcer

Topics: Adenocarcinoma; Carcinoid Tumor; Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Peptic Ulcer; Stomach Neoplasms

Omeprazole, 20 mg every second day, in prevention of duodenal ulcer relapse has been tested. 15 patients with peptic ulcer, which was endoscopically proved and then healed, underwent the treatment. No matter of ulcer original seat as well as antacid drug previously employed, recurrences were not seen after a 6 months period, while clinical symptoms and possible adverse reactions appeared to be very slight. The proposed regimen of omeprazole seems to be cost-saving and worth proving.

Topics: Adult; Aged; Aged, 80 and over; Drug Evaluation; Female; Gastrins; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer; Recurrence; Time Factors

The effects of chronic drug-induced hypergastrinemia on the exocrine and endocrine stomach are still incompletely understood. Chronic hypergastrinemia in rats and humans is associated with gastric argyrophil cell hyperplasia.. Seventy-four patients with chronic ranitidine-resistant ulcerations were treated chronically with omeprazole (median observation period 48 [6-84] months).. Median fasting serum gastrin levels increased from a pretreatment value of 74-145 pg/mL after 3 months. No further increase was observed thereafter. The finding of atrophic gastritis increased from 1.8% to 20.8% after 5 years. A doubling of the mean argyrophil cell volume density (0.36% vs. 0.74% after 5 years; P < 0.01%) was paralleled by a decrease in the normal endocrine cell growth pattern from 64.3% to 33.3% and an increase in micronodular hyperplasia (8.9% vs. 16.7%). These changes correlated with the severity of corpus gastritis and seemed to be more disease- than drug-related. No statistically significant changes were observed in the antral G- and D-cell volume densities under therapy.. Long-term omeprazole therapy in humans results in moderate hypergastrinemia and a significant argyrophil cell hyperplasia, which are correlated to the grade of corpus gastritis. Because hypergastrinemia and gastritis are closely related, it is difficult to quantitatively assess their respective role in this process.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Cell Division; Female; Gastrins; Gastritis; Helicobacter Infections; Helicobacter pylori; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer; Stomach; Time Factors

Recurrent peptic ulcer after gastric surgery differs from duodenal ulcer in that they usually occur with low acid output, which is sufficient to cause ulceration in predisposed stomach or anastomosis. The proton pump inhibitor (PPI), significantly more potent and long-acting than H2-blocker, is expected to be more effective for postoperative recurrent ulcers. We evaluated the efficacy of omeprazole (OPZ) on recurrent ulcers in 12 patients following either gastrectomy or vagotomy. The healing rate after 4 week treatment with OPZ was 58% and increased to 100% after 8 week. Evaluation of quick symptom relief also supported the efficacy of OPZ treatment. These findings showed that OPZ treatment resulted in a more rapid healing of recurrent ulcers compared with H2-blocker. It remains to be clarified whether quit of treatment with PPI would induce high ulcer relapse rates, and whether maintenance therapy with PPI would be the only alternative therapy for surgical intervention.

Topics: Adenosine Triphosphatases; Adult; Aged; Female; Gastrectomy; Gastric Acid; Gastrins; H(+)-K(+)-Exchanging ATPase; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer; Postoperative Complications; Recurrence; Vagotomy

Fasting serum gastrin values were measured by radioimmunoassay in 53 children with peptic ulcer disease. The mean fasting serum gastrin levels for children with chronic duodenal ulcer, acute gastric ulcer, acute duodenal ulcer who were younger than two years old and acute duodenal ulcer who were older than two years old were: 46.2 +/- 25.7 pg/mL, 46.9 +/- 43.5 pg/mL, 47.9 +/- 12.0 pg/mL and 37.5 +/- 17.8 pg/mL, respectively. Children with peptic ulcer disease did not have elevated fasting serum gastrin levels when compared with age-matched controls. We conclude that a fasting serum gastrin value cannot be used as a screening test for peptic ulcer disease in children, except for Zollinger-Ellison syndrome.

Topics: Adolescent; Child; Child, Preschool; Gastrins; Humans; Infant; Peptic Ulcer

Recently, antisecretory drugs such as H2-receptor antagonists (H2-RA) or proton pump inhibitor have been used for peptic ulcer patients widely in Japan. However, there are possibilities that long term administration of H2-RA might cause changes in intragastric environment. The present study was designed to clarify the changes of surgical treatment in Japan Surgical Society training hospitals, before and after introduction of H2-RA. Serum gastrin and antral G-cell number was measured after administration of H2-RA (1 mg/kg 14 days continuous infusion) in rat. Also, acid secretion and gastrin response stimulated by adrenalin (40 ng/kg.min) were measured in duodenal ulcer patients. 1) In the view of surgical treatment, elective operation highly decreased after the introduction of H2-receptor antagonists, and showed the increase of the rate of emergency operation up to 70%. 2) Hypergastrinemia and antral G cell hyperplasia were observed after administration of H2-RA in rats. 3) Acid secretion stimulated by adrenalin which is considered as antral G cell dependent, showed a higher response in H2-RA treated cases than in those untreated. 4) Antrectomy was carried out in 43.4% of the patients treated with H2-RA versus 18.9% to the patients untreated.

Topics: Animals; Cell Count; Famotidine; Gastric Acid; Gastrins; Histamine H2 Antagonists; Humans; Hyperplasia; Interphase; Male; Peptic Ulcer; Pyloric Antrum; Rats; Rats, Wistar; Surveys and Questionnaires

The development of gastric enterochromaffin-like (ECL)-cell hyperplasia in humans may be associated with extreme hypergastrinaemia, as occurs in Zollinger-Ellison syndrome (ZES) and pernicious anaemia (type A gastritis). More recently, endocrine cell hyperplasia has been found in all forms of chronic atrophic gastritis and even in cases of focal atrophy. Serum gastrin levels, non-antral gastric endocrine (argyrophil) cell growth, and the severity and type of concomitant gastritis were monitored in 66 unoperated and 8 antrectomized patients with poorly responsive peptic ulcer or reflux oesophagitis during up to 5 years' treatment with high-dose omeprazole, 40 mg daily. A small subgroup of patients (23%) had serum gastrin concentrations of more than four times the normal upper limit. These patients also had hyperplasia of the gastric argyrophil cells. More importantly, the same subgroup of patients had high-grade (atrophic) gastritis. Micronodular hyperplasia of argyrophil cells was significantly more frequent in biopsies showing atrophic gastritis (48%) than in biopsies showing only superficial gastritis (3.6%). It is concluded that, as previously demonstrated in untreated patients with gastric ulcer, the argyrophil cell hyperplasia observed during high-dose omeprazole therapy is related to the progression of chronic atrophic gastritis rather than to serum gastrin levels.

Topics: Biopsy; Esophagitis, Peptic; Gastric Mucosa; Gastrins; Gastritis, Atrophic; Humans; Hyperplasia; Longitudinal Studies; Omeprazole; Peptic Ulcer; Severity of Illness Index

In a follow-up study operative risk, postoperative functional disorders and incidence of anastomotic (recurrent) ulcer after partial gastrectomy with Roux-en-Y gastrojejunostomy for gastroduodenal ulcer were evaluated in 52 patients. Lethality for elective treatment was 0 and for emergency surgery (ulcer bleeding) 16.7%. 29.5% of the patients reported postoperative functional disorders. Because Roux-en-Y reconstruction prevented duodenogastric reflux, intragastric pH was low (median 2.2) and in the absence of ulcer protective, neutralizing reflux anastomotic ulcer occurred in 15.9% of the patients. With regard to the high rate of recurrent ulcer Roux-en-Y reconstruction after partial gastrectomy for primary ulcer surgery should be avoided and reconstruction procedures preferred, which guarantee duodenogastric reflux.

Topics: Anastomosis, Roux-en-Y; Bile Reflux; Female; Follow-Up Studies; Gastrectomy; Gastric Acidity Determination; Gastrins; Humans; Jejunum; Male; Peptic Ulcer; Postgastrectomy Syndromes; Postoperative Complications; Radiography; Recurrence

The regulation of gastrin secretion from antral G-cells is of major importance in the physiologic control of acid secretion. Gastrin secretion is highly dependent upon gastric intraluminal pH and is inhibited significantly by a pH of less than 3.0. Acute gastric alkalinization greater than pH 6.0 with antisecretory agents such as H2-receptor antagonists or H+/K+ ATPase inhibitors has little impact on fasting serum gastrin levels but promotes an enhanced sustained rise in meal-stimulated gastrin release. Courses of standard therapy with both H2-antagonists and H+/K+ inhibitors cause a significant rise in 24 h integrated plasma gastrin levels that is inversely correlated to the 24-h integrated gastric acidity. The rise in fasting or integrated plasma gastrin levels observed in patients treated with H2-antagonists is small and of unclear clinical significance. Therapy with antisecretory agents leads to earlier ulcer relapse than with other agents. A variety of factors have been proposed to explain the earlier ulcer relapse rate, including secondary hypergastrinemia with rebound acid hypersecretion after discontinuation of the drug. Secondary hypergastrinemia may also lead to tolerance to prolonged courses of H2-antagonists therapy with a decrease in acid inhibition. This may contribute to break-through ulcer recurrence during maintenance H2-antagonist therapy. However, the relative importance of hypergastrinemia and tolerance to H2-antagonists compared with other factors such as baseline gastric acid secretion, smoking status, nonsteroidal anti-inflammatory drug use, and Helicobacter pylori status is difficult to assess.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adenosine Triphosphatases; Carcinoid Tumor; Gastrins; H(+)-K(+)-Exchanging ATPase; Histamine H2 Antagonists; Humans; Peptic Ulcer; Stomach Neoplasms

Topics: Age Factors; Carcinoid Tumor; Esophagitis, Peptic; Female; Gastrins; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer; Risk Factors; Sex Factors; Stomach Neoplasms

Topics: Gastric Acid; Gastrins; Helicobacter Infections; Helicobacter pylori; Humans; Peptic Ulcer

The salient contributions of the Zollinger-Ellison syndrome have made it unique. No pancreatic endocrine tumor described before (insulinoma) or subsequently (glucagonoma, somatostatinoma, vipoma, pancreatic-polypeptidoma) has been the topic of such a variety of studies, or has been such an inspiration and rich source of new ideas for investigation and ultimate improvement in patient care.

Topics: Gastrinoma; Gastrins; Humans; Lymphatic Metastasis; Pancreatic Neoplasms; Peptic Ulcer; Research; Zollinger-Ellison Syndrome

Topics: Age Factors; Aged; Campylobacter; Chronic Disease; Gastric Acid; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Middle Aged; Pepsin A; Peptic Ulcer; Recurrence; Risk Factors

Topics: Autonomic Nervous System; Campylobacter; Cell Cycle; Gastric Acid; Gastric Mucosa; Gastrin-Releasing Peptide; Gastrins; Humans; Microcirculation; Pepsin A; Peptic Ulcer; Peptides; Prostaglandins; Secretin

In 1983, all trials of omeprazole in humans were stopped because rats given the drug developed gastric endocrine cell hyperplasia and carcinoid tumors. Further studies in rats showed that drug-induced achlorhydria and hypergastrinemia caused these changes. Because data in humans are limited, we compared the numbers of endocrine cells, as judged by silver staining (argyrophilia), in the gastric mucosa of patients with Zollinger-Ellison syndrome, who are hypergastrinemic, and in normogastrinemic patients with idiopathic acid-peptic diseases. In addition, we analyzed the number of gastric endocrine cells in patients with Zollinger-Ellison syndrome given omeprazole for up to 3 years. Patients with Zollinger-Ellison syndrome had 15.7% +/- 6.9% argyrophil cells in biopsies of gastric oxyntic mucosa, and patients with idiopathic acid-peptic disease had 7.8% +/- 2.3% (P less than 0.01). In patients with Zollinger-Ellison syndrome, the percentage of argyrophil cells was not related to serum gastrin concentration, duration of symptoms, time since diagnosis, basal or maximal acid output, extent of tumor, or age. There was a tendency for patients with multiple endocrine neoplasia type 1 to have a greater percent of argyrophil cells than patients with sporadic Zollinger-Ellison syndrome. Considering the biopsies from both normogastrinemic and hypergastrinemic patients, there was a significant relationship between the percentage of argyrophil cells and the serum concentration of gastrin (P less than 0.01). Patients with Zollinger-Ellison syndrome given omeprazole for up to 3 years developed no significant changes in percentage of argyrophil cells, no carcinoid tumors, and no changes in serum concentrations of gastrin. The present study shows that patients with Zollinger-Ellison syndrome have an increased percentage of argyrophil cells in oxyntic mucosa and that omeprazole does not increase this percentage. In periods of up to 3 years, omeprazole had no effects on gastric morphology in patients with Zollinger-Ellison syndrome.

Topics: Adult; Cell Count; Female; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Omeprazole; Parietal Cells, Gastric; Peptic Ulcer; Staining and Labeling; Time Factors; Zollinger-Ellison Syndrome

Serum gastrin levels were determined in 120 consecutive patients (43 females, 77 males) with peptic disease 24 h post dose after 4 weeks continuous omeprazole (40 mg daily) treatment. Serum gastrin levels were elevated in 33 (28%) but exceeded the twice normal range in only 6 patients (5%). Age and sex did not influence the magnitude of gastrin levels. Gastrin increments induced by omeprazole compared to pretreatment with H2-blockers in 60 cases were similar in both males (42 +/- 10 pg/ml) and females (44 +/- 9 pg/ml). It is concluded that the magnitude of gastrin increases observed during omeprazole therapy are small and independent of age and sex.

Topics: Adolescent; Adult; Age Factors; Aged; Esophagitis, Peptic; Female; Gastrins; Histamine H2 Antagonists; Humans; Male; Middle Aged; Omeprazole; Peptic Ulcer; Sex Factors

A total of 143 patients with peptic ulceration of the duodenum, stomach and oesophagus who did not respond to 3 or more months of high-dose treatment with ranitidine, 450 mg or more daily, were treated with oral omeprazole, 40 mg daily. In 94% of the patients, ulcers healed within 2-8 weeks. After healing, 133 patients underwent long-term maintenance treatment with omeprazole, 40 mg daily, for 1-5 years (continuing). During maintenance therapy with omeprazole, no endoscopically verified relapses occurred, and no drug-related adverse effects were seen. There were no significant changes in routine laboratory tests in any patient, including 27 with concomitant liver cirrhosis. Basal serum gastrin levels, which were already elevated by the previous high-dose ranitidine treatment, rose to 4 times normal levels after 4 months of treatment with omeprazole. Thereafter, no further increases in basal serum gastrin levels were observed, even after 5 years of administration. The volume density of argyrophilic cells in the oxyntic mucosa increased during omeprazole treatment, but no dysplasia of the gastric enterochromaffin-like cells was seen. In conclusion, omeprazole was highly effective in healing ranitidine-resistant peptic ulcers, and subsequent maintenance therapy with omeprazole, 40 mg daily, was found to be effective and safe over the period observed.

Topics: Drug Resistance; Esophagitis, Peptic; Gastrins; Humans; Omeprazole; Peptic Ulcer; Ranitidine; Time Factors

Serum gastrin was determined in 33 patients during treatment with the proton pump inhibitor omeprazole. After 4 weeks of therapy, gastrin levels increased to a median of 55 pg/ml compared to 15 pg/ml prior to omeprazole (P less than 0.001). There was a close correlation (r = 0.939; P less than 0.001) between pre-treatment gastrin and levels at 4 weeks. Comparison of serum gastrin concentrations at 1 month of omeprazole with levels at 6 (n = 21) and 12 months (n = 12) continuous therapy revealed a close correlation (r = 0.961 and r = 0.882, respectively; P less than 0.001) despite dose adjustment. In marked hypochlorhydria documented by continuous pH monitoring, serum gastrin varied from normal up to profound hypergastrinaemia. These results demonstrate that the serum gastrin increase under powerful acid-inhibitory drug therapy depends upon a number of variables. (a) Only in patients with elevated gastrin levels, prior to omeprazole treatment, can moderate to marked hypergastrinaemia during omeprazole be expected. (b) Gastrin increases reached during the initial period of omeprazole treatment remain constant during long-term therapy. (c) Acid inhibition itself is not necessarily associated with an increase in serum gastrin in every patient, which suggests that the individual sensitivity of the gastrin cell to acid inhibition is more important for serum gastrin changes than the degree of acid inhibition itself.

Topics: Esophagitis, Peptic; Gastric Acid; Gastrins; Humans; Omeprazole; Peptic Ulcer; Radioimmunoassay; Vagotomy

Gastric emptying (GE) of a radiolabeled solid meal, gastric acid secretion and gastrin release were examined within a median of 15.5 days (range: 9 to 66) after surgery in 14 peptic ulcer patients subjected to truncal vagotomy with Cassimally pyloroplasty (VTP-Cas). A significant delay in GE was observed after VTP-Cas; the median slope of GE curves, K, decreased from 14.65 (range: 2.56 to 21.86) before to 4.05 (range: 0 to 11.67) min-1.10-3 after the operation (p less than 0.002). The postoperative GE was significantly slower than in a group of 41 healthy controls (median K = 9.09, range: 3.72 to 28.66 min-1.10(-3), p less than 0.01 vs the VTP-Cas-operated patients), and was characterized by a biphasic pattern with a slowed second phase. VTP-Cas resulted in a reduction of the basal acid secretion by an average of 87% (from 9.5 +/- 3.4 to 1.2 +/- 0.2 mmol.h-1, p less than 0.05), and the pentagastrin-stimulated acid output by 72% (from 30.8 +/- 7.2 to 8.6 +/- 1.6 mmol.h-1, p less than 0.05). The fasting serum gastrin concentration remained unchanged after VTP-Cas (68.2 +/- 10.8 pre- vs 67.3 +/- 9.4 ng.1-1 post-operatively), whereas a slight and statistically insignificant increase in the meal-induced gastrin release was found following the VTP-Cas-AUC0-120: 10002 +/- 1298 pre- vs 11234 +/- 1422 ng.1-1 min postoperatively.

Topics: Adult; Female; Gastric Acid; Gastric Emptying; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Postoperative Period; Pyloric Antrum; Vagotomy, Truncal

In 14 peptic ulcer patients undergoing truncal vagotomy with Heineke-Mikulicz pyloroplasty (VTP-HM), gastric emptying of a radiolabeled solid meal, gastric acid secretion and gastrin release was examined within a median of 14 days (range; 10 to 63 days) following the operation, and compared with the results obtained in 14 patients subjected to vagotomy and Cassimally pyloroplasty (VTP-Cas). VTP-HM markedly disturbed gastric emptying in 10 out of 14 patients (71%), four of which (28%) had extremely rapid, and six (43%) exhibited abnormally delayed gastric emptying. Due to a wide inter-subject variability, no significant differences between VTP-HM and VTP-Cas were found for any of the gastric emptying parameters considered. The basal acid output was significantly lower after VTP-Cas than VTP-HM: 2.4 +/- 0.8 vs 5.8 +/- 1.0mmol.h-1, (p less than 0.02). The difference in pentagastrin-stimulated gastric acid secretion: 9.4 +/- 1.4 vs 12.0 +/- 1.8 mmol.h-1 for VTP-Cas vs VTP-HM, respectively, was not statistically significant. Higher fasting serum gastrin concentration (102.0 +/- 21.1 vs 63.3 +/- 8.3 ng.l-1), and greater postprandial gastrin release (AUC0-120: 16690 +/- 2648 vs 10654 +/- 1283 ng.l-1 min) were observed after VTP-HM than after VTP-Cas. The respective differences did not, however, reach the level of statistical significance, the possible clinical relevance of the differences between the two pyloroplasty procedures with respect to their effect on gastric evacuatory and secretory functions is discussed.

Topics: Adult; Aged; Aged, 80 and over; Female; Gastric Acid; Gastric Emptying; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Postoperative Period; Pyloric Antrum; Vagotomy, Truncal

Topics: Administration, Oral; Biopsy; Child, Preschool; Endoscopy, Gastrointestinal; Female; Gastrins; Humans; Infusions, Intravenous; Omeprazole; Pepsinogens; Peptic Ulcer; Pyloric Antrum; Zollinger-Ellison Syndrome

Bone mineral metabolism was studied in 20 male patients, between 8 and 18 years, after surgical treatment for peptic ulcer (ten Billroth 1 and ten Billroth 2 gastrectomies) and in 16 sex- and aged-matched healthy controls. The bone mineral content was statistically reduced only in the Billroth 2 group. Serum 25(OH)D was lower in all patients, but fractional calcium absorption was similar to the control value. This may be due to increases in 1,25(OH)2D and parathyroid activity (particularly in Billroth 2). Serum osteocalcin levels and hydroxyproline excretion were higher than in the controls. A positive linear correlation emerged not only between serum 1,25(OH)2D and PTH levels but also between each of these and serum osteocalcin and urine hydroxyproline. Both PTH and calcitriol were inversely correlated with the bone mineral mass in Billroth 2, confirming a trend observed in Billroth 1. Although calcitonin values were normal, basal gastrin levels were severely impaired in all patients. In response to a mixed meal, increases in gastrin and calcitonin were significantly lower than in the controls. The calcitonin response to intravenous calcium and pentagastrin infusion was not significantly different to the controls. The percentage increase in gastrin and calcitonin responses to oral calcium correlated positively with the reduction in bone mineral content only in the Billroth 2 group, suggesting a reduction in calcitonin release may contribute to gastric surgery osteopenia in these patients.

Topics: Adolescent; Bone Density; Bone Diseases, Metabolic; Calcitonin; Calcitriol; Child; Gastrectomy; Gastrins; Humans; Male; Parathyroid Hormone; Peptic Ulcer

Both H2-receptor antagonists and pirenzepine are used in the treatment of peptic ulcer disease. Since we have recently found a higher frequency of non-responders to H2-receptor antagonists among cirrhotics, we tested the effect of the combination of 50 mg pirenzepine and 300 mg ranitidine in 25 patients (12 cirrhotics and 13 controls) in whom a normal 300 mg dose of ranitidine had failed to suppress intragastric acidity. Nocturnal intragastric pH was continuously monitored for 12 hours. A rise in the intragastric pH above 4.0 for more than 6 hours following the oral dose at 18.00 h was considered as response. In all subjects, plasma concentrations of ranitidine and pirenzepine were in the therapeutic range. Coadministration of pirenzepine and ranitidine resulted in sufficient increase of the intragastric pH in only 4 of the 12 patients with cirrhosis, and in 4 of the 13 control patients. This treatment failure in most of our patients does not support the view that excessive vagal drive might play an important role in the non-response to H2-blockers. With regard to the benefit resulting from coadministration of pirenzepine and ranitidine, there seems to be no difference between cirrhotic and control patients.

Topics: Adult; Aged; Chromatography, High Pressure Liquid; Circadian Rhythm; Drug Therapy, Combination; Female; Gastric Acidity Determination; Gastrins; Humans; Hydrogen-Ion Concentration; Liver Cirrhosis; Male; Middle Aged; Peptic Ulcer; Pirenzepine; Ranitidine

Apart from the complication of gastrointestinal vasculitis it is not known whether the upper gastrointestinal (UGI) tract has any special disease characteristics in rheumatoid arthritis (RA). However, oesophageal motility disorders have been reported in 30% of RA patients. Hypergastrinaemia has been found in 23-43% of RA patients, usually in combination with a decreased gastric acid output. Another finding suggestive of a decreased secretory state, namely a decreased level of pepsinogen A, was found in RA patients with the sicca syndrome and in patients with active disease. The risk for peptic ulcer disease with regard to nonsteroidal anti-inflammatory drugs (NSAID) is possibly higher in RA patients than in patients with other rheumatic diseases. These findings suggest that in RA patients intrinsic factors play a role in the pathogenesis of the oesophageal motility disorders, in hypergastrinaemia and hypopepsinogenaemia and the related decreased gastric secretory state, and possibly in the increased susceptibility to NSAID-related ulcers. However, there are also indications that oesophageal motility disorders, hypergastrinaemia, and NSAID-related ulcers in RA are the result of extrinsic factors, mainly the use of NSAIDs. The effects of NSAIDs and gold compounds on infection with Helicobacter pylori, a possible pathogenetic factor in ulcer disease, is discussed. It is clear that the discussion about intrinsic and extrinsic factors as a cause of the UGI manifestations in RA remains an intriguing but difficult subject for further studies.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Rheumatoid; Esophageal Diseases; Esophageal Motility Disorders; Gastric Acid; Gastrins; Helicobacter pylori; Humans; Pepsinogens; Peptic Ulcer; Stomach Diseases

We attempted to induce chronic peptic ulcer in the rat by injection of consecutive doses of cysteamine. We investigated the incidence of peptic ulceration and measured gastric mucosal histamine, histamine formation capacity (HFC), plasma gastrin and tissue (oesophagus, duodenum, liver and lung) histamine in rats 1, 7, 14, 21, and 28 days after injection of cysteamine-HCl (300 mg/kg s.c. and 100 mg/kg 8 h later). Saline injections were used in control rats. After 24 h all rats given cysteamine had duodenal ulcers and the ulcer incidences after 7 and 14 days were 60 and 40%, respectively. After Day 21 no ulcers were found. Microscopy revealed ulcer healing seen as epithelialized scars from Day 14 onwards. A rising incidence of gastric metaplasia of the duodenal mucosa was noted from Day 7 after cysteamine treatment, which may have pathophysiological significance. Gastric mucosal histamine was higher and plasma gastrin was lower after 24 h compared with controls and values obtained later in the study. Rats with duodenal ulceration had significantly higher gastric mucosal histamine than those without lesions and control rats. A direct relationship was found between plasma gastrin and HFC in rats given cysteamine. A small but significant increase in histamine content of the liver was also observed after 24 h. No significant changes were found in other tissue specimens. Thus, a rise in gastric histamine is associated with duodenal ulcers in this model.

Topics: Animals; Cysteamine; Duodenum; Female; Gastric Mucosa; Gastrins; Histamine; Intestinal Mucosa; Peptic Ulcer; Rats; Rats, Inbred Strains

We report a patient with severe peptic ulcer disease and a right ovarian mass that was found to be a gastrin-producing cystadenocarcinoma. Gastrin production by the tumor was stimulated by secretin and inhibited by the long-acting somatostatin analogue SMS 201-995. Following resection of the tumor, serum gastrin levels and the gastrin response to secretin returned to normal. Histologic examination, including Alcian blue staining for mucin and immunoperoxidase staining for gastrin, revealed gastrin at the base and mucin at the apex of the tumor cells. This report demonstrates secretin stimulation and somatostatin inhibition of gastrin secretion from a cell that is apparently not of endocrine origin.

Topics: Cystadenocarcinoma; Female; Gastrins; Humans; Immunoenzyme Techniques; Middle Aged; Octreotide; Ovarian Neoplasms; Ovary; Peptic Ulcer; Secretin; Staining and Labeling

The antisecretory and antiulcer activities of 2[[[3-methyl-4-(2,2,2-trifluoroethoxy)-2-pyridyl]methyl] sulfinyl]-1H-benzimidazole (AG-1749) were investigated in dogs and rats. AG-1749 inhibited both the (H+ + K+)-adenosine triphosphatase activity in canine gastric microsomes and dibutyryl cyclic AMP-stimulated acid formation in isolated canine parietal cells and suppressed the acid secretion stimulated by histamine, pentagastrin, bethanechol or a peptone meal in Heidenhain pouch dogs; the ID50 values were between 0.2 and 0.7 mg/kg p.o. AG-1749 inhibited both the histamine-stimulated and the basal acid secretion in pylorusligated rats and prevented water immersion stress or aspirin-induced gastric lesions and mepirizole or cysteamine-induced duodenal ulcers in rats; the ID50 values were between 0.3 to 3.6 mg/kg p.o. or i.d. Furthermore, AG-1749 prevented gastric lesions induced by absolute ethanol or acidified aspirin, and accelerated the healing of acetic acid-induced gastric or duodenal ulcers in rats. The inhibitory potency of AG-1749 in dogs was much the same as that of omeprazole and about half that of ranitidine. However, it was about 2 to 10 times more potent than omeprazole and 4 to 34 times more potent than ranitidine in rats. These results suggest that AG-1749 exerts prominent antiulcer activities mainly by suppressing acid secretion via an inhibition of a proton pump in gastric parietal cells and partly by protecting the gastrointestinal mucosa against various ulcerative stimuli.

Topics: 2-Pyridinylmethylsulfinylbenzimidazoles; Adenosine Triphosphatases; Animals; Anti-Ulcer Agents; Dogs; Gastric Acid; Gastric Mucosa; Gastrins; H(+)-K(+)-Exchanging ATPase; In Vitro Techniques; Lansoprazole; Male; Omeprazole; Pepsin A; Peptic Ulcer; Protons; Rats; Rats, Inbred Strains

Assessment of serum gastrin, digestion and absorption of protein, fat 10-15 days after operative treatment in 119 patients with gastric ulcer revealed that independent of the observation time the gastrin level remains low in patients following gastric resection and high following selective proximal vagotomy. The processes of digestion and absorption of proteins, fats are inhibited in the early period after operative intervention with a tendency towards normalization in the remote period.

Topics: Adult; Digestion; Gastrectomy; Gastric Mucosa; Gastrins; Humans; Intestinal Absorption; Iodine Radioisotopes; Middle Aged; Peptic Ulcer; Postoperative Period; Radionuclide Imaging; Vagotomy, Proximal Gastric

The prevalence of peptic ulcer disease was retrospectively analysed in 35 patients affected by primary hyperparathyroidism consecutively observed from 1977 through 1987. Eight of the examined patients (22.8%) had peptic ulcer (7 duodenal and 1 gastric ulcer), that in five cases (14%) represented the first clinical manifestation of the endocrine disease. A Zollinger-Ellison syndrome was demonstrated in three cases (8.5% of the total series, 37% of the patients with ulcer). There was no difference in calcium, gastrin and parathormone serum level between patients with and without ulcer, excluding patients with Zollinger-Ellison syndrome. These data confirm the high prevalence of peptic ulcer disease in hyperparathyroidism, but the mechanism causing this association remains to be elucidated.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Calcium; Female; Gastrins; Humans; Hyperparathyroidism; Male; Middle Aged; Parathyroid Hormone; Peptic Ulcer; Retrospective Studies; Zollinger-Ellison Syndrome

In this paper, 89 Spleen deficiency (SD) patients' gastric mucosa specimens obtained during fibrogastroscopy mucosal biopsy were observed with immunocytochemical-stereologic-quantitative analysis method. The number of G cells counted and the content of basic gastrin in serum measured. This study found that the difference of the number of G cells and the content of gastrin in serum possessed statistical significance between two types of SD. The results suggested the hyperplasia and hypersecretion of G cells in gastric antrum might be an important pathological mechanism for different types of SD.

Topics: Adolescent; Adult; Aged; Female; Gastric Mucosa; Gastrins; Gastritis; Gastroscopy; Humans; Immunohistochemistry; Male; Medicine, Chinese Traditional; Middle Aged; Peptic Ulcer; Pyloric Antrum; Splenic Diseases

The secretion of gastric acid in the peptic ulcer patients were examined by the dopamine infusion test (DIT). Production of gastric acid was investigated when the patients were treated by 30-minute dopamine infusion of 2 micrograms/kg/min. According to the difference of production of gastric acid, 132 patients were categorized into three groups: 59 Cata-responders, 28 Ana-responders and 45 Non-responders. Cata-responders were the patients whose production was less than 0.2mEq/30 min, Ana-responders, greater than 0.2mEq/30 min and Non-responder less than or equal to 0.2mEq/30 min. Cata- and Ana-responders showed higher gastric acid secretion preoperatively, and higher gastric acid reduction rate after selective proximal vagotomy (SPV) than Non-responder. Cata-responder showed decreased acid output preoperatively and unchanged after SPV with DIT. Ana-responder showed increased acid output preoperatively and decreased after SPV with DIT. Non-responder showed unchanged acid output preoperatively and decreased after SPV. Cata-responder may be depending more on vagus-mediated factor and parietal cell mass. Ana-responder may be depending more on vagus-mediated factor, parietal cell mass and dopaminergic factor. Non-responder may be depending more on gastrin cell mass and less cholinergic influence. From these findings dopamine receptor may exist in the stomach, and DIT seems to be useful in studying pathogenesis of the peptic ulcer and determining treatment for patients with peptic ulcer.

Topics: Adolescent; Adult; Aged; Dopamine; Female; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Infusions, Intravenous; Male; Middle Aged; Peptic Ulcer; Vagotomy, Proximal Gastric

We report a 45-year-old woman with chronic peptic ulcer disease and multiple episodes of bowel obstruction, who was admitted with gastric outlet obstruction. Because of gastric hypersecretion, a diagnosis of Zollinger-Ellison syndrome was suspected and an initial serum gastrin of 1,251 pg/ml supported this diagnosis. Subsequent evaluation failed to reveal a gastrinoma. A repeat serum gastrin level after 14 days of continuous nasogastric decompression was 43 pg/ml, suggesting that the initial hypergastrinemia was due to antral distention. It is important to consider the possibility of gastric outlet obstruction as a stimulus for serum gastrins in the range previously considered diagnostic for the Zollinger-Ellison syndrome.

Topics: Diagnosis, Differential; Female; Gastric Dilatation; Gastrins; Humans; Intestinal Obstruction; Middle Aged; Peptic Ulcer; Pyloric Antrum; Zollinger-Ellison Syndrome

Topics: Adult; Aged; Aged, 80 and over; Anemia, Pernicious; Biopsy; Female; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Somatostatin

Growth hormone-releasing factor (GRF) was reported to possess the growth-promoting action on the gastroduodenal mucosa that can be augmented by removal of endogenous somatostatin. Since mucosal proliferation was considered to contribute to healing of chronic gastroduodenal ulcerations, we designed the study to determine the interaction of GRF and somatostatin on the healing rate of acetic acid-induced chronic gastric and duodenal ulcers and on the growth of gastroduodenal mucosa in rats. GRF injected subcutaneously twice daily at 100 micrograms/kg/day for 7 days resulted in a significant enhancement of healing rate of both gastric and duodenal ulcerations and this was accompanied by a significant increase in the weight of the mucosa and the contents of RNA and DNA. GRF also significantly increased serum gastrin levels and the tissue contents of epidermal growth factor (EGF) in salivary glands, duodenum and pancreas, suggesting that both gastrin and EGF could contribute to mucosal trophic and ulcer healing effects of GRF. Somatostatin (100 micrograms/kg/day for 7 days) abolished almost completely the ulcer healing and mucosal growth-promoting effects of GRF and this was accompanied by the reduction in serum gastrin level and the tissue contents of EGF suggesting that the suppression of gastrin and EGF release could contribute to the observed effects of somatostatin. We conclude that GRF has both the ulcer healing and the mucosal trophic actions which can be antagonized by somatostatin and that gastrin and EGF may be implicated in these actions.

Topics: Acetates; Acetic Acid; Animals; Epidermal Growth Factor; Gastric Mucosa; Gastrins; Growth Hormone-Releasing Hormone; Intestinal Mucosa; Male; Peptic Ulcer; Rats; Somatostatin; Wound Healing

Topics: Gastric Acid; Gastrin-Releasing Peptide; Gastrins; Gastrointestinal Hormones; Humans; Peptic Ulcer; Peptides; Somatostatin

Pathophysiological effects following biliary tract reconstruction for benign biliary diseases were investigated from the standpoint of gastric acid secretion, metabolism of nutrients and gastrointestinal hormone release. Patients undergoing Roux-Y hepaticojejunostomy showed a significant increase in maximum acid output at follow-up, although only one case of peptic ulcer was observed. In addition, the frequency of cases showing gastric acid hypersecretion was higher than for jejunal interposition hepaticoduodenostomy. Two kinds of test meals (carbohydrate-rich or fat-rich) were given, on different days, to each patient before and about four weeks after surgery. Plasma concentrations of gastrointestinal hormones and glucose or triglyceride were determined. Fasting concentrations of gut hormones (gastrin, GIP, insulin and GLI) were similar to those before surgery, and increased after the ingestion of the test meals. Gastrin and total GLI levels tended to be higher in the Roux-Y than in the interposition group, and vice versa for both insulin and GIP. The changes in plasma glucose and triglyceride, following the Roux-Y procedure, suggest disturbances in carbohydrate tolerance, fat digestion, and in the anabolic phase of absorbed fat. Patients undergoing the Roux-Y procedure should be carefully followed up, since gastric acid hypersecretion induced by a postprandial augmented release of gastrin was observed.

Topics: Adult; Aged; Anastomosis, Roux-en-Y; Biliary Tract Surgical Procedures; Blood Glucose; Carbohydrate Metabolism; Fats; Female; Gastric Acid; Gastrins; Gastrointestinal Hormones; Humans; Jejunum; Male; Middle Aged; Peptic Ulcer; Postoperative Complications; Triglycerides

Topics: Animals; Binding, Competitive; Cimetidine; Drug Therapy, Combination; Gastric Acid; Gastrins; Glutamine; Peptic Ulcer; Proglumide; Rats; Receptors, Gastrointestinal Hormone

Gastrin releasing peptide(GRP)-like immunoreactivity in human plasma was measured using radioimmunoassay of neuromedin C (NMC) in 83 healthy and 58 diseased subjects. In the healthy group, the mean value of fasting GRP-like immunoreactivity was 2.1 +/- 1.4 (mean +/- SD) pmol/L. There was a slight positive correlation between the GRP-like immunoreactivity values and aging. Postprandial serial measurements demonstrated that GRP-like immunoreactivity showed no response to a significant elevation of serum gastrin concentration. The group with chronic renal failure on hemodialysis gave the highest value, 7.1 +/- 2.1 pmol/L (p less than 0.01). There were no statistical differences between the healthy controls and groups with peptic ulcer, liver cirrhosis, diabetes mellitus or carcinomas, although some cancer patients had a marked increase in GRP-like immunoreactivity value.

Topics: Adult; Aged; Bombesin; Diabetes Mellitus; Female; Gastrin-Releasing Peptide; Gastrins; Humans; Kidney Failure, Chronic; Liver Cirrhosis; Male; Middle Aged; Neoplasms; Peptic Ulcer; Peptide Fragments; Peptides; Radioimmunoassay

36 patients with chronic gastric or oesophageal peptic ulceration (including 6 with antrectomy), resistant to high-dose ranitidine treatment for at least 3 months, were successfully treated with 40-60 mg of omeprazole daily for periods between 1 and 2 years. Fasting serum gastrin levels were monitored at regular intervals during therapy and multiple gastric mucosal biopsies were taken during gastroscopy every 3-6 months. Gastrin levels increased significantly during the first 6 months of therapy from a medium level of 81.5 to 206 pg/ml, a slight decrease was seen thereafter. In 10 patients investigated before the start of the treatment and after 1 and 2 years, the volume density of argyrophilic cells in the oxyntic mucosa increased from 0.43 +/- 0.08 to 0.91 +/- 0.14% during the first year; this change was statistically significant. No further increase was observed thereafter. No such difference could be demonstrated between a larger group of 18 patients investigated before and after 1 year of treatment with omeprazole (0.806 +/- 0.1 vs. 0.93 +/- 0.08%) and between a larger group of 22 untreated patients and 17 patients treated for 17-24 months with omeprazole (0.73 +/- 0.1 vs. 0.86 +/- 0.09%). The volume density of argyrophilic cells found in 8 patients with gastrinoma amounted to 1.37 +/- 0.22%. No clusters of endocrine cells were found in omeprazole-treated patients. The D cell volume density in the antral mucosa decreased significantly during the first months of treatment, but steadily increased thereafter to reach pretreatment values after 17 months. There was no change in G cell volume density under therapy. No changes in gastrin levels or oxyntic argyrophilic cells were observed in the antrectomized patients. It is concluded that the hyperplasia of argyrophilic cells observed in some patients during long-term omeprazole treatment is mediated by hypergastrinaemia.

Topics: Female; Gastric Mucosa; Gastrins; Humans; Male; Omeprazole; Parietal Cells, Gastric; Peptic Ulcer; Ranitidine; Stomach Ulcer; Time Factors

Topics: Achlorhydria; Antacids; Carcinoid Tumor; Enterochromaffin Cells; Gastrins; Gastritis, Atrophic; Histamine H2 Antagonists; Humans; Hyperplasia; Peptic Ulcer; Risk; Somatostatin; Stomach Neoplasms; Vagotomy, Proximal Gastric

This study describes the model of chronic gastric and duodenal ulcerations induced by the application of acetic acid on a strictly defined area of the serosal surface of the stomach and duodenum for 10 and 20 s, respectively. Acetic acid applied for longer (20-60 s) or on a larger area (28-64 mm2) resulted in the formation of severe ulcerations which penetrated into the surrounding organs and had very prolonged healing time. Ulcers induced by the application of acetic acid for 10-20 s on a smaller area (7-13.8 mm2) healed spontaneously within 2-3 weeks, thus constituting a model suitable for evaluation of drugs affecting the process of ulcer healing. Our preliminary results of 7- to 14-day treatment with certain drugs indicate that sucralfate and De-Nol, at the dose which does not affect gastric acid secretion, accelerated the healing rate of both gastric and duodenal ulcers so that the observed ulcer healing effect could be attributed to their ulcer healing property. In contrast, 16, 16-dimethyl PGE2 (dmPGE2) in cytoprotective dose was completely ineffective in enhancing ulcer healing. Higher, gastric inhibitory dose of dmPGE2 accelerated the healing of duodenal but not gastric ulcerations, indicating that the inhibition of gastric secretion rather that cytoprotective activity is responsible for ulcer healing effect of this prostaglandin.

Topics: Animals; Bismuth; Chronic Disease; Dinoprostone; Disease Models, Animal; Gastric Acid; Gastric Mucosa; Gastrins; Male; Pepsin A; Peptic Ulcer; Prostaglandins E; Rats; Rats, Inbred Strains; Sucralfate

The aim of this study was to determine whether mucosal antrectomy, which preserves antropyloric motility, would enhance the antiulcer properties of proximal gastric vagotomy (PGV). Hydrochloric acid and gastrin secretion were studied in five dogs before and after PGV and mucosal antrectomy, while the response to the Mann-Williamson operation (an ulcer-producing operation) was evaluated in four control dogs with intact stomachs, five dogs with PGV alone, and six dogs with PGV plus mucosal antrectomy. Proximal gastric vagotomy and mucosal antrectomy decreased mean +/- SEM basal and pentagastrin-stimulated acid secretion from 4.3 +/- 1.3 to 0.4 +/- 0.3 mEq/hr and from 21 +/- 0.7 to 7.4 +/- 1.8 mEq/hr, respectively (p less than 0.05). Basal plasma gastrin was altered little by the operation (68 +/- 9.7 pg/ml before, 58 +/- 11 pg/ml after; p greater than 0.05) but the 4-hour integrated plasma gastrin response to a 200 gm meat meal decreased from 13 +/- 1.8 to 3.3 +/- 0.7 ng X min/ml (p less than 0.05). Only one of six dogs with mucosal antrectomy and PGV developed peptic ulcer after the Mann-Williamson operation, whereas four of five with PGV alone and three of four controls developed ulcers (p less than 0.05, PGV alone versus PGV and mucosal antrectomy). In conclusion, PGV and mucosal antrectomy decreased acid secretion and postcibal gastrin response and provided greater protection against peptic ulcer than PGV alone.

Topics: Animals; Dogs; Evaluation Studies as Topic; Female; Gastric Acid; Gastric Mucosa; Gastrins; Jejunal Diseases; Male; Peptic Ulcer; Postoperative Complications; Pyloric Antrum; Vagotomy, Proximal Gastric

Topics: Circadian Rhythm; Duodenal Ulcer; Gastrins; Humans; Pepsinogens; Peptic Ulcer; Stomach Ulcer

The role of endogenous gastrin in the pathogenesis of "idiopathic" ulcer disease is difficult to determine; however, gastrin is probably only of limited importance besides various probable more important factors. In conditions associated with uncontrolled gastrin production by a gastrin secreting tumor or in cases in which the feedback regulation between gastrin release and intragastric pH is disturbed severe and recurrent ulcers may develop. Radioimmunological determination of serum gastrin levels enable to identify such cases of ulcer disease due to an excess of circulating gastrin.

Topics: Gastric Acid; Gastrins; Humans; Pancreatic Neoplasms; Peptic Ulcer; Recurrence; Zollinger-Ellison Syndrome

Topics: Adult; Aged; Duodenum; Female; Gastric Mucosa; Gastrins; Hepatitis, Alcoholic; Hepatitis, Chronic; Humans; Liver Cirrhosis; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Peptic Ulcer; Stomach

Management of patients with multiple endocrine neoplasia type I (Wermer's syndrome) who have concurrent hypercalcemia and hypergastrinemia is controversial. The usual therapeutic approach has been to perform parathyroidectomy first before surgery for ulcer disease in an effort to decrease serum calcium concentration and presumably remove one of the stimuli for both gastrin and gastric acid secretion. We present the history of a 48-year-old man with primary hyperparathyroidism and Zollinger-Ellison syndrome who underwent acid secretory studies and secretin stimulation tests before and after parathyroidectomy. We also studied the effect of calcium channel blockade on gastrin and gastric acid secretion, since calcium influx into endocrine cells, such as the gastrinoma cell, is thought to be critical in hormone secretion. Although parathyroidectomy reduced serum calcium and parathormone levels to normal, basal serum gastrin concentration and basal acid output remained unchanged. The peak rise in serum gastrin concentration after secretin injection was less after parathyroidectomy than before parathyroidectomy but was still abnormal. During administration of verapamil, a calcium channel antagonist, no change was seen in the serum gastrin concentration, secretin test response, or acid secretion. Basal acid output was 45.4 mmol/hr before parathyroidectomy or verapamil and 54.0 and 50.4 mmol/hr after parathyroidectomy or verapamil, respectively. In contrast, a small but significant decrease (p less than 0.05) in serum parathormone concentration occurred during treatment with verapamil, an observation that to the best of our knowledge has not been previously reported in humans.

Topics: Calcium Channel Blockers; Gastric Acid; Gastrins; Humans; Hyperparathyroidism; Male; Middle Aged; Parathyroid Glands; Pedigree; Peptic Ulcer; Verapamil; Zollinger-Ellison Syndrome

Topics: Adult; Aged; Fasting; Female; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Renal Dialysis; Renal Insufficiency

It is argued that all chronic gastroduodenal peptic ulcers result from localised increase in mucosal susceptibility to acid attack at the interface between a segment of gastroduodenitis and gastric fundus or duodenal mucosa. The site is predetermined by the background mucosal pattern. Changes can occur in the differentiated gastroduodenal mucosa that closely resemble cell population transformations described in embryology and regeneration biology. A second pathological process, gastroduodenitis, may develop that does not of itself predispose to ulceration, but the combination of factors can produce a zone of increased acid susceptibility. These complex changes could be generated by immunologically activated gastroduodenitis. Destructive or stimulatory immune reactions, analogous to those seen in the thyroid gland, could affect the gastrin-secreting G cells and other paracrine cells. The resulting tropic and inflammatory reactions would provide the background for peptic ulceration.

Topics: Autoantibodies; Chronic Disease; Duodenitis; Duodenum; Gastric Fundus; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Intestinal Mucosa; Parietal Cells, Gastric; Peptic Ulcer; Zollinger-Ellison Syndrome

Between 1971 and 1983, 31 males and 13 females were found to have peptic ulceration associated with hypergastrinaemia. An antral G-cell lesion was present in 11 (25 per cent) and a gastrinoma in 14 (32 per cent). There were 11 patients with multiple endocrine adenomatosis (MEA) (25 per cent) and 4 (9 per cent) with primary hyperparathyroidism. Four patients (9 per cent) were unclassified. Length of history and level of gastrin did not differentiate between the groups and an average of 2.5 operations was performed per patient, while the overall mortality was 27.3 per cent. The patients with G-cell lesions were significantly younger than all the other groups (P less than 0.01). Partial gastrectomy adequately treated G-cell hyperplasia. Total gastrectomy was required to treat pancreatic gastrinomata but additional pancreatic resection did not improve the outcome. In MEA, parathyroidectomy did not influence the treatment of a gastrinoma. This is the first recorded experience of surgery for hypergastrinaemia in the United Kingdom and the outcome of such a retrospective study may be a guide to the future management of these conditions.

Topics: Adenoma, Islet Cell; Adolescent; Adult; Aged; Female; Gastrectomy; Gastrins; Humans; Hyperparathyroidism; Male; Middle Aged; Multiple Endocrine Neoplasia; Pancreatectomy; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

The localization of immunoreactive calcitonin (IR-CT) in the human gastric mucosa and tumor tissues was studied using an immunohistochemical peroxidase-antiperoxidase method. A small number of IR-CT-containing cells were observed in both infant and adult gastric antral mucosa and the ratio of IR-CT-containing cells to G cells was about 1:50-100. Moreover, tissue content of IR-CT in normal antral mucosa was 2.37 +/- 0.35 ng/g wet weight. IR-CT-containing cells and G cells decreased with the progress of chronic atrophic gastritis and were totally absent in intestinal metaplastic glands. IR-CT was detected in G cells, suggesting a paracrine relation between gastrin and CT. IR-CT was not found in tumor cells of 35 gastric adenomas and 40 well differentiated adenocarcinomas. On the other hand, it was demonstrated in a very small number of tumor cells in 4 of 46 poorly differentiated adenocarcinomas, and in a good number in 3 of 7 scirrhous argyrophil cell carcinomas. IR-CT in plasma could serve, therefore, as a tumor marker of scirrhous endocrine cell carcinoma, and its production in cancer cells was considered to be eutopic rather than ectopic.

Topics: Adenocarcinoma, Scirrhous; Adenoma; Adult; Aged; Calcitonin; Female; Gastric Mucosa; Gastrins; Humans; Immunoenzyme Techniques; Infant; Male; Microscopy, Electron; Middle Aged; Peptic Ulcer; Pregnancy; Stomach Neoplasms; Tissue Distribution

As effective tumour resection can be achieved in only a minority of patients with Zollinger-Ellison syndrome, therapy in such patients is usually directed to treatment and prevention of symptoms induced by hypersecretion of gastric acid. Omeprazole is a potent and long-acting inhibitor of pentagastrin stimulated gastric acid secretion in normal subjects, and this prompted a study of the effect of omeprazole on gastric acid hypersecretion and acid peptic disease resulting from endogenous hypergastrinaemia in Zollinger-Ellison patients. Omeprazole was found to be effective even in those patients whose symptoms were not adequately controlled by high doses of histamine H2-receptor antagonists, with or without pirenzepine. Serum gastrin levels were not affected; no laboratory abnormalities and minimal side-effects induced by omeprazole have been reported in Zollinger-Ellison patients even on long-term studies of up to 27 months.

Topics: Anti-Ulcer Agents; Benzimidazoles; Gastric Acid; Gastrins; Humans; Omeprazole; Peptic Ulcer; Time Factors; Zollinger-Ellison Syndrome

Topics: Gastric Acid; Gastric Mucosa; Gastrins; Humans; Muscle, Smooth; Peptic Ulcer; Receptors, Cell Surface; Receptors, Cholecystokinin; Stomach Neoplasms

This study was designed to test the effects of pentagastrin and epidermal growth factor (EGF) on stress-induced ulceration and on the antral content of gastrin and somatostatin (SLI) in rats. Four groups of 14 to 15 rats had been prepared for 7 days by one of the following methods: saline injection (control); injection of pentagastrin (250 micrograms/kg, 3 times/day); injection of EGF (10 micrograms/kg, 3 times/day); or injection of EGF plus pentagastrin. At the end of the treatment period, half of each group of rats were sacrificed (nonstress group). There were no ulcers in the nonstress control groups of rats. Stress was applied by water immersion in the remaining half of the rats. The injections of pentagastrin and/or EGF resulted in substantial increase in antral content of SLI. After 20 hours of stress, the ulcer index was 40.5 +/- 3.3 in the controls, compared to 6.4 +/- 1.2 and 16.2 +/- 2.3 in rats that received pentagastrin or EGF, respectively. Injections of both pentagastrin and EGF resulted in an ulcer index of 26.2 +/- 2.0, which was significantly lower than that in controls, but higher than that in rats treated with either peptide alone. The stress resulted in significant decrease in antral SLI in all groups of rats, whereas SLI content in rats treated with pentagastrin and/or EGF remained significantly higher than that of controls. Antral content of gastrin did not differ significantly in the four groups tested. The ulcer index was inversely correlated with antral SLI content. We confirm and extend previous observations that pentagastrin and EGF prevent stress ulcer formation, and suggest that endogenous SLI may account, at least in part, for their antiulcer activity.

Topics: Animals; Epidermal Growth Factor; Gastrins; Immersion; Male; Pentagastrin; Peptic Ulcer; Radioimmunoassay; Rats; Rats, Inbred Strains; Somatostatin; Stomach; Stress, Physiological

The endocrine pancreas from four hypergastrinemic patients with recurrent peptic ulceration has been studied by light and electron microscopy. Greatly increased numbers of ducts and centroacinar cells have been observed associated with a striking increase in the number of islets and endocrine cells scattered in the acinar tissue (nesidioblastosis). The islet cells scattered throughout the exocrine parenchyma are of all the known islet cell types, with a prevalence of B and especially A cells. Many islets, probably formed de novo, are of a considerable size, have irregular contours and are in close apposition to centroacinar cells and ducts. The degree of nesidioblastosis and islet hyperplasia does not seem to be related to the plasma gastrin levels. Cytological changes have also been found in the islet cells of the hypergastrinemic patients compared with controls. These changes mainly affect the B cells and consist of a striking decrease in the number of mature secretory granules associated with a fairly extended ergastoplasm and Golgi apparatus and with a relevant increase in the number of immature granules. In two of the four patients examined, who had more severe hypergastrinemia, cytological signs of enhanced secretion are also recognized in A cells. The features indicating hypersecretion of B and A cells seem to be related to the plasma gastrin levels. The above findings indicate that chronic endogenous hypergastrinemia promotes proliferation and differentiation of islet cells and stimulates the secretory function of B cells and, to a lesser extent, of A cells, thus providing evidence for a trophic and secretagogue action of gastrin on the endocrine pancreas.

Topics: Female; Gastrins; Humans; Islets of Langerhans; Male; Microscopy, Electron; Middle Aged; Pancreatic Diseases; Peptic Ulcer

Topics: Gastrins; Gastritis, Atrophic; Gastrointestinal Diseases; Humans; Peptic Ulcer; Radioimmunoassay; Stomach Neoplasms

Topics: Adolescent; Adult; Aged; Female; Gastric Acidity Determination; Gastrins; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Peptic Ulcer; Stress, Physiological

The article describes 44 observations of peptic ulcers, the appearance of them being explained by the retained antral mucosa in the stump of the duodenum and stomach.

Topics: Calcium; Gastrectomy; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Postoperative Complications; Secretin; Zollinger-Ellison Syndrome

Topics: Adult; Aged; Calcium; Female; Gastrins; Humans; Infusions, Parenteral; Injections, Intravenous; Iodine; Male; Middle Aged; Peptic Ulcer; Secretin; Zollinger-Ellison Syndrome

Heterogeneity is the most important consideration in the pathophysiology of peptic ulcer disease. Acute ulcers and erosions present clinically with gastrointestinal bleeding or perforation. If they heal there is no predictable recurrence. Factors concerned with mucosal defense are relatively more important than aggressive factors such as acid and pepsin. Local ischemia is the earliest recognizable gross lesion. The gastric mucosa is at least as vulnerable as the duodenal mucosa and probably more so. Most drug-induced ulcers occur in the stomach. Chronic or recurrent true peptic ulcers (penetrating the muscularis mucosae) usually present with abdominal pain. Many duodenal ulcer patients report that the pain occurs when the stomach is empty or is relieved by food, and follows a pattern of relatively long periods of freedom from symptoms between recurrences. Approximately 50% of patients experience a recurrence within a year if anti-ulcer medication is stopped. In most western countries recurrent duodenal ulcer is more common than gastric ulcer. Peptic ulcer disease is also more common in men. Recent evidence indicates genetic and familial factors in duodenal ulcer and increased acid-pepsin secretion in response to a variety of stimuli. However, it is also becoming clear that of all the abnormal functions noted, few are present in all subjects and many are clustered in subgroups. In chronic gastric ulcer of the corpus, defective defense mechanisms, such as duodenogastric reflux and atrophic gastritis, seem to be more important than aggressive factors. Nevertheless, antisecretory medications accelerate the healing of such ulcers. It remains to be seen whether prostaglandins, mucus secretion, or gastric mucosal blood flow are impaired in chronic ulcer disease.

Topics: Acute Disease; Animals; Burns; Chronic Disease; Duodenal Ulcer; Gastric Acid; Gastric Emptying; Gastrins; Humans; Intestinal Mucosa; Peptic Ulcer; Recurrence; Spinal Cord Injuries; Stomach Ulcer; Stress, Physiological

Topics: Adult; Female; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Secretin

Topics: Animals; Cell Count; Gastric Mucosa; Gastrins; Humans; Mast Cells; Peptic Ulcer; Rats; Time Factors; Vagotomy

A consecutive series of 357 endoscopic gastric biopsies was investigated after staining of histological sections with the Grimelius silver method. Argyrophil cells were classified according to the type of mucosa (fundic, antropyloric or intestinalized) in which they were located. Cases of argyrophil cell hyperplasia detectable on a qualitative basis were selected and their associations with various gastroduodenal disorders of the patients as well as with functional and pathological findings of the gastric mucosa were investigated. Hyperplasia of fundic argyrophil cells was more frequent in patients with atrophic gastritis of the fundic mucosa and a relatively well preserved antral mucosa as well as in patients with hyperplastic polyps. In contrast, it was infrequent in patients with duodenal ulcer and gastric stump. Hyperplasia of antropyloric argyrophil (non-G) cells was most frequent in patients with gastric peptic ulcer or with hyperplastic polyps as well as in those with atrophic gastritis of the fundic mucosa irrespective of the concomitant condition of antral mucosa. Hyperplasia of metaplastic argyrophil cells was more frequent in intestinal metaplasia of the antral mucosa than in that of fundic mucosa. Moreover, it was more frequent in patients with gastric cancer.

Topics: Adolescent; Adult; Aged; Biopsy; Female; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Diseases; Gastroscopy; Humans; Hyperplasia; Intestinal Mucosa; Male; Metaplasia; Middle Aged; Peptic Ulcer; Polyps; Silver; Staining and Labeling; Stomach Neoplasms

Topics: Adolescent; Adult; Aged; Female; Gastrins; Humans; Kidney Failure, Chronic; Male; Middle Aged; Peptic Ulcer; Ranitidine; Renal Dialysis

Topics: Diazepam; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Pepsin A; Peptic Ulcer

Using the bile duct ligated (BDL) pig as a model of experimental peptic ulceration, a study was made of the effects of highly selective vagotomy (HSV) upon basal and stimulated acid and pepsin secretion, tissue levels of n-acetylglucosaminidase, prostaglandins (PgE2) and gastrin, and gastric venous plasma gastrin. In addition to reducing basal acid and pepsin output, HSV was found to return towards normal the elevated tissue prostaglandin and depressed antral gastrin levels after BDL. In addition, it was observed that gastric juice specimens were markedly viscid. It is suggested that there may be effects of HSV other than acid and pepsin reduction which require attention.

Topics: Acetylglucosaminidase; Animals; Dinoprostone; Disease Models, Animal; Female; Gastric Acid; Gastric Mucosa; Gastrins; Lysosomes; Pepsin A; Peptic Ulcer; Prostaglandins E; Swine; Vagotomy, Proximal Gastric

Topics: Adult; Calcium; Female; Gastrectomy; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Middle Aged; Motilin; Peptic Ulcer; Secretin; Zollinger-Ellison Syndrome

Topics: Adolescent; Adult; Age Factors; Aged; Gastric Acid; Gastrins; Humans; Middle Aged; Peptic Ulcer; Sex Factors

Topics: Adult; Cell Count; Gastrins; Humans; Middle Aged; Peptic Ulcer; Pyloric Antrum

Topics: Adenocarcinoma; Adult; Aged; Female; Gastric Mucosa; Gastrins; Gastrointestinal Diseases; Humans; Male; Middle Aged; Peptic Ulcer; Peptide Fragments; Protein Precursors; Pyloric Antrum; Stomach Neoplasms

Topics: Administration, Oral; Female; Gastrectomy; Gastric Acidity Determination; Gastrins; Glycine; Humans; Male; Middle Aged; Peptic Ulcer; Stomach Neoplasms

Primary gastrin cell hyperfunction of the gastric antrum as a clinical syndrome consists of basal hypergastrinemia, an exaggerated gastrin response to feeding, the absence of any ectopic source of gastrin secretion, and peptic ulcer disease. The number of G-cells were quantitated in the gastric antrum of five patients with clinically diagnosed primary G-cell hyperfunction, and the results were compared to controls with a variety of gastric diseases. Patients with the clinical diagnosis of primary G-cell hyperfunction had a significantly increased number of antral G-cells (p less than 0.05). The clinical syndrome of primary G-cell hyperplasia appears to be associated with hyperplasia of G-cells rather than with the hypersecretion of gastrin by a normal number of G-cells.

Topics: Adult; Chromaffin System; Diagnosis, Differential; Enterochromaffin Cells; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Hyperplasia; Male; Middle Aged; Peptic Ulcer; Pyloric Antrum; Stomach Diseases; Syndrome; Zollinger-Ellison Syndrome

Topics: Adult; Female; Gastrectomy; Gastric Acid; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Recurrence; Zollinger-Ellison Syndrome

The functional and morphological effects of duodeno-gastric reflux have been studied in the dog. Reflux causes hypersecretion of acid to pentagastrin and a hypergastrinaemic response to a standard meal, associated with antral gland hyperplasia. It is suggested that these changes are mediated by suppressed somatostatin activity, and that they may play an important part in the pathogenesis of peptic ulceration.

Topics: Animals; Disease Models, Animal; Dogs; Dose-Response Relationship, Drug; Duodenal Diseases; Duodenum; Gastric Acid; Gastric Mucosa; Gastrins; Histamine; Male; Pentagastrin; Peptic Ulcer; Somatostatin; Stomach; Stomach Diseases

This paper reports a personal experience in the management of 45 patients with recurrent ulcer after gastric surgery. Inadequate acid reduction was the major cause of ulcer recurrence and treatment was by further acid reduction. Revisional surgery was performed in 23 patients (including a patient with a gastro-jejuno-colic fistula) with one mortality. Preliminary results of therapy with histamine H2-receptor antagonists have been encouraging and there appears to be a reduced need for re-operation in these patients in recent years. Less common causes of ulcer recurrence include retained suture material (2 cases) and the Zollinger-Ellison syndrome (2 cases). The incidence of post-surgical ulcer recurrence may be reduced by: improved surgical techniques, particularly in the performance of vagotomy, and avoidance of operations without acid reducing procedures e.g., gastro-jejunostomy without vagotomy; wider use of emergency ulcer curative surgery for perforated peptic ulcer. Experience at two local centres has been that this is a safe procedure in selected patients, there being no mortality in 58 cases. Routine screening of peptic ulcer patients for the Zollinger-Ellison Syndrome by measuring the serum gastrin level facilitates early diagnosis of the condition, thus forestalling gastric surgery and the inevitable recurrent ulceration.

Topics: Combined Modality Therapy; Duodenal Ulcer; Female; Gastrectomy; Gastrins; Histamine H2 Antagonists; Humans; Male; Middle Aged; Pentagastrin; Peptic Ulcer; Peptic Ulcer Perforation; Recurrence; Vagotomy; Zollinger-Ellison Syndrome

Topics: Aspirin; Bile Acids and Salts; Gastric Acid; Gastric Emptying; Gastric Inhibitory Polypeptide; Gastrins; Histamine Release; Humans; Indomethacin; Mast Cells; Peptic Ulcer; Somatostatin

There are few detailed studies of patients with pathological hypergastrinaemia of antral origin. We have identified four patients with severe acid hypersecretion associated with peptic ulcer disease and in whom no evidence for gastrinoma or isolated retained antrum could be found. Three of these patients also had hypergastrinaemia. In two patients, one with gastric ulcers and one with duodenal ulcer disease, the hypergastrinaemia appeared to be due to antral gastrin cell hyperfunction and there was also evidence for mild antral gastrin cell hyperplasia. In the other hypergastrinaemic patient, a primary intestinal gastrin cell hyperfunction syndrome was suspected, but a hidden gastrinoma could not be excluded. The remaining patient had nearly fatal hypersecretory ulcer disease and cimetidine failed to control the hypersecretory state. In this patient the hypersecretion responded to a more potent H2 antagonist with resolution of a metabolic encephalopathy. No general pathophysiological mechanism could be identified in these patients or in larger groups of patients with gastric or duodenal ulcer disease.

Topics: Adult; Aged; Duodenal Ulcer; Duodenum; Gastric Acid; Gastrins; Humans; Male; Peptic Ulcer; Pyloric Antrum; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Adult; Aged; Female; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Postgastrectomy Syndromes; Zollinger-Ellison Syndrome

The prevalence of gastrinomas and the Zollinger-Ellison syndrome is unknown. In order to examine a high risk group of patients, basal and secretin-provoked plasma gastrin levels were determined in 50 consecutive patients, predominantly from the west of Scotland. All had endoscopically proven recurrent peptic ulceration following duodenal ulcer surgery. This resulted in three cases strongly suspected of having a gastrinoma. Further investigations including exploratory laparotomy were unable to demonstrate a gastrinoma in two, but the evidence suggested an occult tumour in one. In this remaining unoperated patient, the serum gastrin returned to normal. The reference range for both basal and secretin stimulated gastrin response and percentage change has been determined in normal control subjects (n = 10) and in primary ulcer patients (n = 20). It is concluded that in this study, gastrinomas had a less than 2 per cent prevalence in patients presenting with recurrent peptic ulceration. As the diagnosis of a gastrinoma changes the surgical approach, conducting screening tests still seems warranted.

Topics: Adolescent; Adult; Aged; Duodenal Ulcer; Female; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Recurrence; Scotland; Secretin; Zollinger-Ellison Syndrome

The secretory and motor function of the stomach and gastrin incretion were investigated in 68 patients with peptic ulcer of variable localization. In addition, a retrospective analysis of the course of prepyloric gastric ulcer and Billroth I resection was performed in 62 patients. Results show that gastric acid secretion and velocity of gastric emptying diminish significantly with increasing height of the localization of the ulcer. Prepyloric gastric ulcer cannot be likened to the duodenal ulcer. Moreover, experimental and clinical results suggest that prepyloric ulcer represents a disease entity per se requiring separate therapeutic approaches (gastric resection following Billroth I).

Topics: Adult; Aged; Duodenal Ulcer; Female; Gastrectomy; Gastric Acid; Gastric Emptying; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Stomach Ulcer

Two brothers with pachydermoperiostosis, an autosomal dominant syndrome characterized by digital clubbing, periosteal new bone formation, coarse facial features with thick, furrowed, and oily skin, presented in their twenties with severe complicated duodenal ulcer disease requiring multiple operations. Their father and one paternal uncle also had pachydermoperiostosis and a past history of ulcer dyspepsia. The mother, one sister, two maternal aunts, and one other paternal uncle were healthy. Both brothers had giant hypertrophic gastritis (Ménétrier's disease). Their pentagastrin-stimulated acid output and fasting and meal-stimulated serum gastrin levels were normal, but their serum pepsinogen I and II levels were markedly elevated. The father had hypochlorhydria and a low serum pepsinogen I/II ratio, suggesting atrophic gastritis. This family study raises the possibility that pachydermoperiostosis, hypertrophic gastropathy, and peptic ulcer may be genetically related.

Topics: Adult; Aged; Dyspepsia; Facial Expression; Female; Gastric Acidity Determination; Gastrins; Gastritis; Gastritis, Hypertrophic; Genes, Dominant; Humans; Male; Middle Aged; Osteoarthropathy, Primary Hypertrophic; Pepsinogens; Peptic Ulcer; Skin Diseases; Syndrome

A possible protective effect of lithium against the occurrence of peptic ulcer complaints in manic-depressive patients, treated with lithium, was investigated. 167 manic-depressive patients, 91 in lithium treatment, 76 not in lithium treatment, were questioned about clinical symptoms of peptic ulcer. Thirteen of the lithium-treated and 23 of the non-lithium-treated patients reported symptoms of peptic ulcer. The difference was statistically significant. The hypothesis that lithium treatment reduces the frequency of symptoms of peptic ulcer in manic-depressive patients was thus confirmed.

Topics: Bipolar Disorder; Gastrins; Humans; Lithium; Peptic Ulcer

The mucosa of the proximal stomach contains a powerful inhibitor of acid secretion and gastrin release. The release of this inhibitor is dependent on intact vagal innervation of the proximal stomach. Thus, proximal gastric vagotomy interferes with the release of the inhibitor. After proximal gastric vagotomy for peptic ulcer, recurrence rates increase over time. In addition, there is some recovery of acid secretion. Although nerve regeneration or sprouting has been suggested as the possible explanation for these events, we propose that interference with the inhibitory mechanism of the proximal stomach may be another possible explanation for the increasing ulcer recurrence rates after proximal gastric vagotomy. At present, this is only a hypothesis and is suggested only by indirect evidence. Direct testing of the hypothesis will require complete purification of the inhibitor and the development of a specific radioimmunoassay.

Topics: Animals; Dogs; Duodenal Ulcer; Gastric Acid; Gastric Fundus; Gastrins; Humans; Peptic Ulcer; Recurrence; Vagotomy; Vagotomy, Proximal Gastric

Topics: Calcitonin; Gastrins; Humans; Liver Diseases; Peptic Ulcer; Time Factors; Zollinger-Ellison Syndrome

Topics: Adult; Female; Gastric Mucosa; Gastrins; Humans; Male; Peptic Ulcer; Somatostatin

Topics: Dumping Syndrome; Gastrins; Glucose; Humans; Hyperglycemia; Hypoglycemia; Peptic Ulcer

The radioimmunoassay technique, first developed for the determination of hormones, has been applied to many substances of biologic interest by clinical and research laboratories around the world. It has had an enormous effect in medicine and biology as a diagnostic tool, a guide to therapy, and a probe for the fine structure of biologic systems. For instance, the assays of insulin, gastrin, secretin, prolactin, and certain tissue-specific enzymes have been invaluable in patient care. Further refinements of current methods, as well as the emergence of new immunoassay techniques, are expected to enhance precision, specificity, reliability, and convenience of the radioimmunoassay in both clinical and research laboratories.

Topics: Acid Phosphatase; Amylases; Animals; Cimetidine; Creatine Kinase; Dogs; Female; Gastrins; Hexosaminidases; Hormones, Ectopic; Humans; Hyperthyroidism; Insulin; L-Lactate Dehydrogenase; Middle Aged; Pancreatic Elastase; Pepsinogens; Peptic Ulcer; Peptides; Pituitary Neoplasms; Prolactin; Radioimmunoassay; Secretin; Species Specificity; Swine; Thyrotropin; Thyrotropin-Releasing Hormone

Topics: Fluorescent Antibody Technique; Gastric Mucosa; Gastrins; Humans; Hyperplasia; Peptic Ulcer; Pyloric Antrum; Stomach Diseases; Zollinger-Ellison Syndrome

Topics: Cell Division; Female; Gastrins; Gastritis; Humans; Immunoenzyme Techniques; Male; Microscopy, Electron; Middle Aged; Peptic Ulcer; Pyloric Antrum

In 26 patients with Roux-Y choledochojejunostomy and 10 with jejunal interposition choledochoduodenostomy, gastrin-stimulated gastric acid secretion and serum levels of gastrin and secretin after feeding were examined before operation and at the time of follow-up. The follow-up levels of maximum acid output were higher than those before operation in each group, and they tended to be higher in patients with Roux-Y choledochojejunostomy (Group I) than in those with jejunal interposition choledochoduodenostomy (Group II), but the difference was not significant. There was no instance of postoperative peptic ulcer in either group. The levels of serum gastrin after feeding tended to be higher in Group II, whereas serum secretin levels were contrarily higher in Group I. The changes in these hormones could be considered not as the cause but rather as the outcome of the changes in postoperative gastric acid secretion.

Topics: Adult; Aged; Biliary Tract; Biliary Tract Diseases; Biliary Tract Surgical Procedures; Duodenum; Gastric Acid; Gastrins; Humans; Jejunum; Middle Aged; Peptic Ulcer; Postoperative Period

After an exposition of the modern trends on the definition, ethiopathogenesis, symptomatology and therapy of the Zollinger-Ellison Syndrome, the authors presents a case of Z.-E. Syndrome, which occurred to their observation.

Topics: Cimetidine; Gastric Juice; Gastric Mucosa; Gastrins; Gastroscopy; Humans; Peptic Ulcer; Zollinger-Ellison Syndrome

This report tests in men the effect of Pirenzepine on L-Amino acids stimulated gastric secretion and serum gastrin levels in order to evaluate the true antimuscarinic selective properties of this drug. Since L-Amino acids given intravenously stimulate gastric acid secretion by a mechanism of action selective on the cholinergic receptors of the gastric parietal cells, not mediated through the vagus nerve, gastrin or other gut hormones. Pirenzepine should be an L-Amino acids antagonist as far as the gastric acid secretion is concerned. By confirming this presumed antagonism between Pirenzepine and L-Amino acids given intravenously, this report points out in men the selective antimuscarinic effect of this anti ulcer drug on the high affinity muscarinic receptors of the gastric parietal cells. Finally a decrease in gastrin serum levels was observed after the i.v. administration of Pirenzepine and this could be explained by a possible effect of blockade of this drug on the cholinergic receptors of the antral G cells, but these data need further experimental confirm. Attention is then paid to the different mechanism of action between Pirenzepine, H2 receptors antagonist drugs and other anti ulcer drugs on healing gastric or duodenal peptic ulcers.

Topics: Amino Acids; Benzodiazepinones; Female; Gastric Acid; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Peptic Ulcer; Pirenzepine; Time Factors

Topics: Blood Glucose; Gastrins; Humans; Insulin; Peptic Ulcer

The effects of jejunal ulcer and chronic endogenous hypergastrinemia on canine gastrointestinal myoelectric activity were investigated in three groups of dogs. All dogs were chronically implanted with electrodes on the stomach and either the duodenum or jejunum. Fasted-state myoelectric activity was monitored before and after gastroenterostomy. Two groups of dogs underwent autotransplantation of the gastric antrum to the midcolon with either gastroduodenostomy or gastrojejunostomy. The third group of dogs underwent diversion of the antroduodenum with gastrojejunostomy. Chronic hypergastrinemia was observed postoperatively in the dogs of each of the three models. Only dogs with gastrojejunostomy and antrocolic transplant developed intestinal ulcers. None of the dogs, despite the presence of ulcers in one group, demonstrated significant changes in myoelectric activity. In both gastrojejunostomy models, a trend toward lengthened interdigesive phase 2 at the expense of phase 1 was seen. No other myoelectric changes were observed and chronic hypergastrinemia had no effect on myoelectric activity in these models. We conclude; (a) experimental jejunal peptic ulcer is not marked by significant changes in interdigestive myoelectric activity and (b) chronic hypergastrinemia is not accompanied by the gastrointestinal muscle, effects reported after acute treatment with gastrin, suggesting a tolerance.

Topics: Animals; Dogs; Electrophysiology; Female; Gastrins; Gastrointestinal Motility; Jejunal Diseases; Male; Muscle Contraction; Muscle, Smooth; Peptic Ulcer

The course of gastric acid secretion and serum gastrin level before and after operation was studied in 41 patients suffering from a gastroscopically determined ulcer disease. In 15 patients suffering from duodenal ulcer, a highly selective vagotomy without pyloroplasty was performed and in 26 patients suffering from peptic ulcer (duodenal or gastric ulcer) a partial gastrectomy (Billroth I). After a highly selective vagotomy without pyloroplasty a reduction in the secretory response to pentagastrin and a significant rise of the basic and postprandial gastrin concentration could be observed. Both methods are suitable to determine the completeness of vagotomy. The estimation of the course of serum gastrin level after vagotomy only reveals a temporary disorder of the antrum-pylorus mechanism. In our opinion a pyloroplasty is not necessary.

Topics: Adult; Duodenal Ulcer; Gastrectomy; Gastric Acid; Gastrins; Humans; Middle Aged; Peptic Ulcer; Pyloric Antrum; Stomach Ulcer; Vagotomy; Vagotomy, Proximal Gastric

Topics: Adult; Diagnosis, Differential; Female; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Portal Vein; Pyloric Antrum; Pylorus; Secretin; Vagotomy; Zollinger-Ellison Syndrome

In order to explore secretory mechanisms in peptic ulcer, the plasma secretin response to an intraduodenal load of gastric acid stimulated with tetragastrin was studied in 10 patients with duodenal ulcer, nine with gastric ulcer, and five young healthy volunteers. After the injection of tetragastrin plasma secretin level was significantly increased in all subjects. The integrated incremental secretin output significantly correlated with the incremental acid output in the duodenal ulcer group as well as the gastric ulcer group. THere was no significant difference in the integrated incremental secretin output among the three groups. However, the integrated incremental secretin output per unit amount of gastric acid loaded in the duodenum was significantly lower in the duodenal ulcer group than in the other two groups. These results suggest that in patients with duodenal ulcer the secretin release in response to an intraduodenal load of endogenous acid is impaired.

Topics: Adult; Duodenal Ulcer; Duodenum; Female; Gastric Acid; Gastrins; Humans; Hydrochloric Acid; Male; Middle Aged; Peptic Ulcer; Secretin; Stomach Ulcer; Tetragastrin; Time Factors

Topics: Aged; Female; Gastrins; Humans; Hypercalcemia; Hyperparathyroidism; Peptic Ulcer

Long-term follow-up of children with the Zollinger-Ellison syndrome (gastrinomas) suggests that surgical management is still advantageous. Twenty-eight children with the Zollinger-Ellison syndrome have been followed up to 21 years after their initial surgical procedure. Six of seven children with less than total gastrectomy, all of whom underwent operation before the introduction of histamine H2-receptor antagonists, are known dead from complications of continued gastric hypersecretion and tumor growth. Sixteen children had a total gastrectomy, with no operative deaths, and only one died of progressive tumor growth, even though 14 had evidence of metastatic islet-cell carcinoma. Follow-up serum gastrin measurements have been obtained for 13 patients with total gastrectomy, and 5 patients now have a normal serum gastrin levels. Malignant gastrinomas in children have been slow growing, indolent, and compatible with long life. The biologic behavior of malignant gastrinomas appears to be more favorable in the young patient. Total gastrectomy can be done safely in children with the Zollinger-Ellison syndrome and effectively controls gastric hypersecretion when all gastrin-producing tumor cannot be excised. Surgical exploration and an attempt at "curative" tumor excision, even when tumor is extrapancreatic and in lymph nodes, appear worthwhile in selected patients.

Topics: Adolescent; Age Factors; Child; Child, Preschool; Cimetidine; Female; Follow-Up Studies; Gastrectomy; Gastric Acid; Gastrins; Humans; Male; Peptic Ulcer; Zollinger-Ellison Syndrome

Despite the increasing awareness of gastrinoma and its lethal peptic ulcer sequelae, the diagnosis is often initially missed or made as a terminal event. The authors screened all patients with peptic ulcer symptoms serious enough to warrant hospital admission or those associated with diarrhea, nephrolithiasis, hypercalcemia, or pituitary abnormality. In a one-year period (1979-1980) nine (of 14 suspected) new gastrinoma patients were identified using a sensitive and specific gastrin radioimmunoassay in combination with provocative tests including IV secretin, calcium, and food. Conventional upper GI series, CAT scan, arteriography, and endoscopy provided no additional information other than to confirm the presence of ulcer disease. Basal plasma gastrin levels were more than 200 pmol L-1 in only three of the nine (normal fasting plasma gastrin levels are less than 25 pmol L-1). Three patients presented with acute ulcer perforation, and the diagnosis of gastrinoma was suspected because of multiple ulcers and pancreatic masses. In three other patients, previous duodenal ulcer surgery had failed. One patient with dyspepsia, high basal plasma gastrin, negative secretin and calcium infusion studies, and a positive meal test was diagnosed as having G-cell hyperplasia; this was confirmed by biopsy and antral gastrin extraction. Antrectomy alone resulted in cure. In all patients tested, a positive calcium infusion or secretin bolus (greater than 100% rise over basal) strongly suggested the diagnosis of gastrinoma, which was confirmed at surgery. In the acute perforations, initial management with omental patch and cimetidine therapy allowed survival of two patients, while emergency total gastrectomy in the third resulted in death due to esophagojejunal leak. Elective patients were treated with cimetidine initially for at least two weeks before total gastrectomy. In this group there were no operative mortalities, and postoperative morbidity was minimal. This series illustrates three important points: (1) careful screening of an ulcer population using gastrin radioimmunoassay and provocative tests has enabled a high yield of gastrinomas while conventional investigations are of minimal values; (2) a high index of suspicion in appropriate cases is necessary; and (3) total gastrectomy performed under elective circumstances is safe and allows the patients to resume a normal and healthy life without the sequelae of aggressive peptic ulceration or daily drug administration

Topics: Adult; Calcium Gluconate; Diagnosis, Differential; Female; Gastrectomy; Gastrins; Humans; Male; Peptic Ulcer; Secretin; Zollinger-Ellison Syndrome

Topics: Antacids; Calcium; Calcium Carbonate; Dose-Response Relationship, Drug; Gastric Acid; Gastrins; Humans; Hydrogen-Ion Concentration; Magnesium Hydroxide; Peptic Ulcer; Stimulation, Chemical

Topics: Adult; Female; Gastric Acid; Gastrins; Gastrointestinal Diseases; Humans; Male; Middle Aged; Peptic Ulcer; Pyloric Antrum; Stomach Neoplasms

Topics: Adult; Female; Gastrectomy; Gastric Acidity Determination; Gastrins; Gastroenterostomy; Humans; Male; Middle Aged; Peptic Ulcer; Postgastrectomy Syndromes; Reoperation; Vagotomy

Topics: Dumping Syndrome; Gastric Acid; Gastrins; Gastroenterostomy; Humans; Peptic Ulcer; Postgastrectomy Syndromes

The development of peptic ulcer surgery is traced from 1881 and Billroth until the present. Discussion of the physiologic basis for gastric resection, the several types of vagotomy, and antrectomy is presented as conceived by the surgeons who originated these operations. Treatment of the complications of peptic ulcer surgery is discussed as well as the current diagnostic and therapeutic approach to the Zollinger-Ellison syndrome.

Topics: Animals; Dogs; Drainage; Duodenal Diseases; Gastrins; History, 19th Century; History, 20th Century; Humans; Intestinal Perforation; Jejunum; Peptic Ulcer; Pyloric Antrum; Stomach; Vagotomy; Zollinger-Ellison Syndrome

Topics: Adolescent; Adult; Aged; Female; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Reagent Kits, Diagnostic

Topics: Gastrins; Humans; Passive Cutaneous Anaphylaxis; Peptic Ulcer; Secretin; Skin Tests

Topics: Adult; Diagnosis, Differential; Female; Gastrins; Humans; Hyperplasia; Peptic Ulcer; Pyloric Antrum; Zollinger-Ellison Syndrome

Topics: Animals; Antacids; Carbenoxolone; Cimetidine; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Stress, Physiological; Vitamin A

Topics: Gastrins; Glucagon; Humans; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Adult; Female; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Pyloric Antrum

Topics: Adult; Chronic Disease; Female; Gastrins; Humans; Male; Middle Aged; Pepsinogens; Peptic Ulcer; Renal Dialysis; Uremia

Topics: Arginine; Gastrins; Growth Hormone; Humans; Injections, Intravenous; Peptic Ulcer; Sulpiride

Measurements of basal and stimulated gastric acid secretion, serum gastrin, and serum pepsinogen I cannot replace direct radiologic and endoscopic examination of the gastroduodenal mucosa for diagnosis of peptic ulcer disease, or histological examination for classification of gastritis and duodenitis. These tests, however, can provide information about the functional status of the gastric mucosa and sometimes indicate the etiology of gastric acid hypersecretion. The most diagnostic combination of tests comprises markedly increased fasting serum gastrin, positive serum gastrin response to secretin challenge, and increased levels of basal acid secretion and serum pepsinogen I found in patients with gastrinoma. The same combination of results, except for negative response to secretin and marked stimulation of gastrin by food, is found in patients with antral gastrin cell hyperfunction. Increased serum gastrin concentrations often are found in patients with hyposecretion of gastric acid, including those with atrophic gastritis, and in patients with renal failure, or previous vagotomy. Patients with atrophic gastritis have a low serum pepsinogen I level, while an increased level is found with renal failure and a normal level is found after vagotomy. Thus, the concurrent measurement of serum pepsinogen I and creatinine provides a useful initial step in the evaluation of hypergastrinemia.

Topics: Creatinine; Duodenitis; Gastric Acid; Gastrins; Gastritis; Humans; Pepsinogens; Peptic Ulcer; Radioimmunoassay; Secretin

Gastric fistula rats (n = 79) were either left as unstressed (fistula closed) controls or gastric secretion, microcirculation (MBF), mucosal stress ulcers were studied in secretory rats subjected to zero (= freely movements allowed), mild, severe restraint stress for 8 h. In all rats gastrin in portal vein and aorta was measured in addition after discontinuation of either protocol. Acid secretion and MBF are progressively reduced by increasing stress. Pepsin and sodium are elevated with severe, acid concentration with mild stress. Pepsin and sodium are elevated with severe, acid concentration with mild stress. Serum gastrin (controls - aorta 53+/- SEM 5, portal vein 73 +/- 9 pg/ml) rises sharply in portal and systemic blood with institution of acid diversion via the outside (zero stress - 136 +/- 21, 398 +/- 98 pg/ml), but declines with increasing stress (severe stress - 82 +/- 16, 101 +/- 27 pg/ml) despite otherwise identical experimental conditions. It is concluded that (1) acid secretion rate and MBF are lowered by stress, but stress ulcers are associated with either increased acidity (mild stress) or peptic activity (severe stress) of gastric juice in the absence of elevated gastrin, (2) enhanced sodium fluxes via gastric lumen and lower acid suggest disruption if mucosal barrier by severe stress, and (3) restraint stress ulcers may be the expression of a combination of disturbances, mainly of metabolic and endocrine nature.

Topics: Animals; Aorta; Gastric Juice; Gastric Mucosa; Gastrins; Male; Peptic Ulcer; Portal Vein; Rats; Rats, Inbred Strains; Regional Blood Flow; Stress, Physiological

In 36 patients with verified hyperparathyroidism (HPT), serum gastrin and its response to secretin was studied before and after parathyroidectomy. In most of the patients gastric secretion-basal acid output (BAO) and maximal acid output (MAO)--was also studied. Seventeen patients had increased serum gastrin values preoperatively and/or postoperatively. Most of the serum gastrin increases were moderate and all but one of the patients with values above 250 pmol/l had hypochlorhydria. Nine patients had a positive secretin test according to conventional criteria preoperatively or postoperatively, but showed no other signs suggestive of a gastrin-producing tumour. Most of the patients with a serum gastrin increase after injection of secretin had hypochlorhydria or achlorhydria. The BAO/MAO ratio was less than 0.6 in all patients. The results of this study do not support the view that primary HPT is often associated with a gastrin-producing tumour as part of a multiple endocrine adenomatosis (MEA type I), but indicate that the observed hypergastrinemia in HPT is almost exclusively related to hypo- or achlorhydria. The findings also give reason to doubt the value of the secretin test.

Topics: Adenoma; Female; Gastric Acid; Gastrins; Humans; Hyperparathyroidism; Male; Middle Aged; Parathyroid Neoplasms; Peptic Ulcer; Secretin

To determine the frequency of gastrointestinal symptoms in primary hyperparathyroidism, we retrospectively analyzed 100 consecutive patients seen at Emory University Hospital from Jan 1, 1977 through March 1, 1979. At the time of diagnosis, 28 patients complained of nausea, 19 of vomiting, 29 of abdominal pain, and 33 of constipation. One patient presented with acute pancreatitis and 14 had ulcer disease (two gastric and 12 duodenal ulcers). Hypercalcemia increases gastric acid secretion and may account for associated ulcer disease and the ulcer-like pain in primary hyperparathyroidism. The mechanisms causing the other gastrointestinal symptoms in hypercalcemia remain to be elucidated. These symptoms abate on correction of hyperparathyroidism.

Topics: Constipation; Female; Gastrins; Gastrointestinal Diseases; Humans; Hypercalcemia; Hyperparathyroidism; Male; Pancreatitis; Peptic Ulcer

Topics: Adolescent; Adult; Aged; Animals; Blood Group Antigens; Child; Coronary Disease; Disease Models, Animal; Disease Susceptibility; Diseases in Twins; Ethnicity; Female; Gastric Emptying; Gastrins; Genetic Markers; Humans; Kidney Calculi; Lung Diseases; Male; Mice; Mice, Inbred NZB; Middle Aged; Models, Genetic; Multiple Endocrine Neoplasia; Pepsinogens; Peptic Ulcer; Urticaria Pigmentosa; Zollinger-Ellison Syndrome

Topics: Female; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Radioimmunoassay; Somatostatin

A review of 42 patients with gastrinoma, who either survived five years or longer or who died during this period of evaluation, was carried out to define the surgical principles which might be combined with the recent trend toward cimetidine therapy. Thirty-four (80%) of the patients had total gastrectomy with an operative mortality rate of 2.3%, and eight patients (20%) had less than total gastrectomy. No tumor was found in six patients with hypergastrinemia and an abnormal secretin bolus whose five-year survival rate was 100%. Of the thirty-six patients having tissue proof of gastrinoma, twenty-two (61%) had complete resection of all gross tumor resulting in a 76% five-year survival rate. Fourteen patients had unresectable tumor or partial resection with a five-year survival rate of 21%. Complete gross tumor resection increased mean survival by six years (p < 0.01), but resulted in persistent eugastrinemia in only two patients. Long-term survival was possible with a combination of vagotomy, lesser gastric procedures, tumor resection, and cimetidine, seven of eight patients living more than five years. Surgical management of gastrinoma should be directed toward aggressive tumor resection and vagotomy, with reliance on cimetidine therapy postoperatively to control the gastric hypersecretion. Total gastrectomy should be reserved for cimetidine failures and those who do not wish to take cimetidine for the rest of their lives.

Topics: Adenoma, Islet Cell; Cimetidine; Follow-Up Studies; Gastrectomy; Gastrins; Humans; Jejunal Diseases; Pancreatectomy; Pancreatic Neoplasms; Peptic Ulcer; Vagotomy

The effect of intravenous secretin on plasma immunoreactive gastrin is presumed to improve diagnostic accuracy in patients with a gastrinoma. To investigate this further, the secretin provocation test was performed in control patients (n = 10), patients with a primary duodenal ulcer (n = 10), patients who had previously had surgery for a duodenal ulcer (n = 20), patients with symptomatic recurrent peptic ulceration (n = 50) and 2 patients with a histologically proved gastrinoma. It was found that the secretin test gave a false positive result in 3 out of 10 symptomatic duodenal ulcer patients, 2 out of 20 patients who had had previous duodenal ulcer surgery and were now asymptomatic and 15 out of 50 patients with recurrent peptic ulceration. Both gastrinoma patients had positive secretin tests but there were no obvious criteria that separated the gastrin response of a gastrinoma patient from those with primary or recurrent peptic ulceration. It is concluded that the secretin test is probably of little value in both the screening and the diagnosis of a gastrinoma.

Topics: Adenoma, Islet Cell; Diagnosis, Differential; Duodenal Ulcer; Gastrins; Humans; Pancreatic Neoplasms; Peptic Ulcer; Recurrence; Secretin

We have studied the relationships between the main molecular forms of gastrin (G17 and G34) in the serum, antral and duodenal mucosa of duodenal (DU) and gastric (GU) ulcer patients. Fasting serum G17 was similar in both DU and GU (about 6 pmol/l) and in both groups increased about three-fold with feeding. In contrast, basal serum G34 was significantly higher in GU (29 pmol/l) than in DU (12 pmol/l) and the peak post prandial increase over basal of G34 was also higher in GU (57 pmol/l) compared with DU (10 pmol/l). In sharp contrast, in the same groups of DU and GU patients mean total antral gastrin concentrations were similar (about 12 nmol/g), and in both groups 95% of antral gastrin was G17, most of the remainder being G34. In both groups total duodenal gastrin concentrations were about 20% those in antral mucosa and about 70% of duodenal gastrin was attributable to G34. The higher serum G34 in GU could therefore be explained by increased secretion of duodenal gastrin, but further work is needed to examine whether there might also be preferential secretion of antral G34 in GU, or a difference in the metabolism (or volume of distribution) of gastrin variants in GU and DU.

Topics: Adult; Aged; Chromatography, Gel; Duodenal Ulcer; Duodenum; Fasting; Female; Gastrins; Humans; Intestinal Mucosa; Male; Middle Aged; Peptic Ulcer; Pyloric Antrum; Radioimmunoassay

Topics: Child; Chronic Disease; Duodenitis; Fasting; Feeding Behavior; Female; Gastrins; Gastritis; Humans; Insulin; Male; Peptic Ulcer; Time Factors

Topics: Adult; Aged; Cell Count; Female; Gastrins; Humans; Immunoenzyme Techniques; Male; Middle Aged; Peptic Ulcer; Stomach

Topics: Adenocarcinoma; Gastrins; Gastritis; Humans; Peptic Ulcer; Radioimmunoassay; Stomach Neoplasms

Serum gastrins and secretion of gastric acid were determined in one patient with recurrent ulcer following a Billroth II gastrectomy with incomplete excision of gastric antrum. Antral exclusion resulted in a modest rise in serum gastrin from 86 pg/ml to 141 pg/ml. This rise in gastrin seemed responsible for an augmented Basal production of acid and the ulcer diathesis as excision of the antral remnant 18 months later resulted in normogastrinaemia, normal gastric acid secretion and disappearance of the ulcer diathesis.

Topics: Adult; Gastrectomy; Gastric Acid; Gastrins; Humans; Male; Peptic Ulcer; Pyloric Antrum; Recurrence; Secretory Rate

In large groups of control subjects and gastric, prepyloric, and duodenal ulcer patients basal gastrin concentration as basal and maximal acid output was measured. All groups had equal basal gastrin concentrations, except gastric ulcer patients, who had higher values (p less than 0.001). A significant negative correlation was found between acid output and basal gastrin in controls and prepyloric ulcer patients. In duodenal ulcer a similar correlation was seen only after exclusion of gastrin and basal acid hypersecretors, and in gastric ulcer no correlation could be found. The characteristic pattern for gastrin and acid secretion was in prepyloric ulcer patients almost like that in controls, whereas gastric ulcer patients seemed more heterogeneous. In duodenal ulcer differences may be explained by a defective feedback inhibition of acid.

Topics: Adolescent; Adult; Aged; Duodenal Ulcer; Female; Gastric Acid; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Stomach Ulcer

Topics: Gastric Juice; Gastrins; Humans; Liver Diseases; Peptic Ulcer

Topics: Adult; Chronic Disease; Duodenal Ulcer; Gastrins; Humans; Middle Aged; Peptic Ulcer; Postgastrectomy Syndromes; Postoperative Period

Topics: Achlorhydria; Calcium; Gastrins; Humans; Molecular Weight; Pentagastrin; Peptic Ulcer; Pyloric Antrum; Zollinger-Ellison Syndrome

Records of 151 patients from the years 1964--1979 with anastomotic ulcers including relapses of ulcers after vagotomy reveal a total lethality of 3.3 per cent after reoperation. Re-gastrectomy with or without additional vagotomy shows a lethality of 5.7 per cent. If vagotomy alone is carried out there were no lethality and nearly no serious complications. Gastrectomy because of recurrent peptic ulcer after primary vagotomy has also no lethality. With regard to less serious postoperative complications including lethality after vagotomy instead of re-gastrectomy we should favour vagotomy for re-operation. Our further examinations will show whether this attitude is justified by long-term results after re-operation of the stomach in consequence of recurrent pepti ulcer.

Topics: Adult; Female; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Recurrence; Splenectomy; Vagotomy

Topics: Adult; Dietary Carbohydrates; Dietary Fats; Dietary Proteins; Female; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Adult; Gastrins; Humans; Male; Peptic Ulcer; Pyloric Antrum; Zollinger-Ellison Syndrome

The relationship between histopathological alterations and G-cell population in the stomach was studied in l4 resected stomachs from patients with chronic peptic ulcer disease (6 with duodenal ulcer and 8 with gastric ulcer). G-cells were identified by indirect immunoperoxidase method. When atrophy was graded three steps (0, 1, 2), the average grade of DU and GU was 0.23 and 0.89, respectively. There was a significant correlation (r=0.871, p less than 0.005) between atropic grade and G-cell population in each stomach. The mean occupation rate with intestinal metaplasia was 0.9% in DU and 35.8% in GU. There was no correlation between total pyloric area and G-cell population, however residual pyloric area excluding intestinal metaplasia correlated significantly with G-cell population (r=0.557, p less than 0.05). There was a significant difference in the mean G-cell population which were 26.5 millions in DU and 8.9 millions in GU. The mean integrated gastrin response to Cimetidine-OXO test meal were 559+/-236 pg/ml in DU and 216+/-124 pg/ml in GU, and there was significant correlation (r=0.889, p less than 0.005) between G-cell population and integrated gastrin response. The average age of both groups, however, was 27.7 in DU and 52.8 in GU, so that these differences of G-cell population and functional G-cell mass in both groups might originate in the histopathological alterations accompanying with the aging.

Topics: Adolescent; Adult; Aged; Chromaffin System; Cimetidine; Duodenal Ulcer; Enterochromaffin Cells; Gastric Mucosa; Gastrins; Guanidines; Humans; Middle Aged; Peptic Ulcer; Pylorus; Stomach; Stomach Ulcer

Maintenance of rats on total parenteral nutrition for 10 days increased the susceptibility of these animals to gastric ulceration and death due to cold-temperature restraint stress. Animals fed the identical diet orally were much less susceptible. Serum gastrin concentrations were increased by stress in both groups of animals despite initially low serum levels. Glucosamine synthetase specific activity was not altered by the method of feeding but tended to be decreased by restraint. These results suggest that orally administered food protects the animal from stress-induced damage by a mechanism(s) involving neither dietary composition nor gastrin.

Topics: Animals; Feeding Behavior; Gastric Mucosa; Gastrins; Male; Peptic Ulcer; Rats

Topics: Adult; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Pyloric Antrum; Recurrence; Vagotomy

Topics: Dumping Syndrome; Gastric Acid; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Postgastrectomy Syndromes; Pyloric Stenosis; Stomach Neoplasms

The causal relationship of primary hyperparathyroidism and ulcer disease is reviewed. In contrast to earlier ideas careful clinical and clinico-chemical investigations have shown that in patients with manifest primary hyperparathyroidism neither is the incidence of ulcer disease raised nor are deviations from the normal behavior of acid secretion or the serum gastrin level to be observed in comparison with the average population.

Topics: Calcium; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hyperparathyroidism; Peptic Ulcer

Recent clinical experiences with 34 Z-E patients indicates that the clinical features and course of the syndrome is less dramatic than described originally. Eighty-five per cent of the patients presented stories of abdominal complaints lasting more than five years and resembling the complaints presented by duodenal ulcer patients (DU). Ulcers were present in 91 per cent of the patients. Fifty-one per cent had either ectopic or multiple ulcers. One third had a single duodenal ulcer resembling an ordinary ulcer. No patients died from complications to the ulcer diathesis. Marked hypersecretion of acid and gastrin was present in the ZE group (BAO:33.7 +/- 7.4; PAO:62.8 +/- 6.1 meq H+/h; gastrin: 5094 pmol/l), but because of great individual variation in the ZE, some overlapping with the acid and gastrin measurements of the DU was seen. The diagnostic value of provocative tests using secretin, calcium, glucagon and food stimulations demonstrated a considerable overlapping between the two groups, indicating that these tests are of little clinical value. Tumours were found in half the patients, revealing malignancy in ten. The ZE can be diagnosed in most cases by combining symptomatology, with measurements of acid and gastrin.

Topics: Adult; Aged; Calcium; Female; Food; Gastric Juice; Gastrins; Glucagon; Humans; Male; Middle Aged; Peptic Ulcer; Secretin; Zollinger-Ellison Syndrome

Topics: Adolescent; Child; Chronic Disease; Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Pepsin A; Peptic Ulcer

Topics: Adolescent; Animals; Gastrectomy; Gastric Juice; Gastrins; Humans; Hyperplasia; Male; Middle Aged; Peptic Ulcer; Pyloric Antrum; Vagotomy; Zollinger-Ellison Syndrome

Nine patients with chronic obstructive pulmonary disease were given oral aminophylline, intravenous aminophylline, and various inhaled and oral adrenergic bronchodilators to determine the effect of these agents on gastric acid secretion and gastrin release. Inhaled epinephrine hydrochloride resulted in an increase in basal acid output of borderline significance (.05 less than P less than .10). Oral aminophylline caused a significant increase in basal acid output from 2.43 to 4.06 mEq (P less than .05). Intravenous aminophylline also caused a significant increase in basal acid output from 0.66 to 2.19 mEq (P less than .01). There were no statistically significant changes in serum gastrin levels after administration of any of the bronchodilators. Aminophylline should be used with caution, if at all, in patients with peptic ulcer disease. In these patients, a beta agonist should be used for initial therapy. If the addition of aminophylline is necessary, antacids should be given.

Topics: Administration, Oral; Aminophylline; Bronchodilator Agents; Gastric Juice; Gastrins; Humans; Infusions, Parenteral; Lung Diseases, Obstructive; Male; Peptic Ulcer

Topics: Adult; Aged; Female; Gastric Emptying; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Recurrence

Topics: Animals; Anura; Bombesin; Dogs; Duodenal Ulcer; Gastrins; Gastritis; Gastrointestinal Diseases; Humans; Peptic Ulcer; Peptides; Stomach Ulcer; Zollinger-Ellison Syndrome

Thirteen patients with Zollinger-Ellison syndrome (ZES) were treated with cimetidine. This population could be divided into chronic forms, mostly presenting as a common duodenal ulcer, and acute forms resulting in critical problems requiring intensive medical care. Among the 7 patients with chronic ZES, cimetidine treatment was unsuccessful in 2; satisfactory clinical control was obtained in 3 others, but gastrinoma excision was the final treatment; cimetidine treatment has been prolonged for more than 15 months in the last 2 patients. If, in this condition, acute pharmacologic secretory inhibition were constantly obtained, therapeutic efficiency criteria are not sensitive enough to establish certainty in the patient's long-term follow-up. Total gastrectomy is still a valuable alternative if excision of the gastrinoma is not possible. Of the 6 patients with acute ZES, 4 were treated by pirenzepin (0.5 mg/kg intramuscularly 3 times a day) adjunctive to cimetidine infusion (2.4 mg/day), which resulted in increased antisecretory activity. However, total gastrectomy was the final outcome in every patient, with 1 immediate postoperative death. In conclusion, cimetidine in ZES treatment, although capable of inducing ulcer healing, diarrhea disappearance, and dramatic secretory inhibition, is still challenged by surgery, which allows either complete cure of the gastrinoma or definitive suppression of the secretory virulence.

Topics: Acute Disease; Benzodiazepines; Chronic Disease; Cimetidine; Duodenal Neoplasms; Gastrectomy; Gastrins; Guanidines; Humans; Peptic Ulcer; Piperazines; Zollinger-Ellison Syndrome

Topics: Adult; Aged; Arginine; Blood Glucose; Female; Gastrins; Glucagon; Homeostasis; Humans; Insulin; Male; Middle Aged; Peptic Ulcer

Topics: Duodenitis; Esophagitis, Peptic; Female; Gastrins; Gastritis; Humans; Male; Peptic Ulcer; Postgastrectomy Syndromes; Stomach Diseases; Stomach Neoplasms

Topics: Adult; Aged; Anti-Ulcer Agents; Benzhydryl Compounds; Biphenyl Compounds; Female; Gastrins; Histamine H2 Antagonists; Humans; Male; Middle Aged; Parasympatholytics; Peptic Ulcer; Propylamines

Topics: Acetylcholine; Cimetidine; Gastric Juice; Gastrins; Guanidines; Histamine; Histamine H2 Antagonists; Humans; Peptic Ulcer; Vagus Nerve; Zollinger-Ellison Syndrome

Topics: Chlorides; Gastric Juice; Gastrins; Gastrointestinal Diseases; Histamine; Humans; Hydrogen; Hydrogen-Ion Concentration; Pentagastrin; Peptic Ulcer; Sodium

Topics: Adult; Aged; Cell Count; Duodenal Ulcer; Female; Fluorescent Antibody Technique; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastrins; Histocytochemistry; Humans; Male; Middle Aged; Peptic Ulcer; Pyloric Antrum; Staining and Labeling; Stomach; Stomach Neoplasms; Stomach Ulcer; Uremia

Topics: Animals; Biliary Tract Diseases; Chemistry; Cyclic AMP; Gastric Juice; Gastric Mucosa; Gastrins; History, 20th Century; Humans; Peptic Ulcer; Prostaglandins; Prostaglandins E; Prostaglandins E, Synthetic

Bromocriptine was administered to 2 subjects with gastrin-secreting tumors of the pancreas. The absorption of the drug was confirmed by a rise in growth hormone levels but no change in the elevated serum gastrin levels were observed. Bromocriptine does not appear to affect gastrin hypersecretion in the way that it influences the hypersecretion of pituitary hormones.

Topics: Adenoma; Adenoma, Islet Cell; Adult; Bromocriptine; Gastrins; Growth Hormone; Humans; Male; Middle Aged; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

The effect of Mucaine and Aludrox on basal and food stimulated immunoreactive gastrin has been assessed in normal control subjects and patients with duodenal or gastric ulcer. No differences in gastrin responses were observed either in the basal period or after the protein meal with the two antacids. As previously described, release of gastrin was greatest in gastric ulcer patients but in contrast to previous results,normal subjects seemed to show a greater response than duodenal ulcer patients but this was not statistically significant. Thus the combination of a local anaesthetic oxethazaine with aluminium hydroxide gel does not lead to diminished gastrin release and is not the prime mechanism of action of this agent.

Topics: Adult; Aged; Aluminum Hydroxide; Antacids; Duodenal Ulcer; Ethanolamines; Gastrins; Humans; Middle Aged; Peptic Ulcer; Stomach Ulcer

The total number of gastric and duodenal gastrin cells was determined in the gastrectomy specimens from eight patients with peptic ulcer. Planimetry was used to determine the antral and duodenal surface. The immunoperoxydase method with specific antigastrin antibodies was used for staining gastrin cells, and the mean concentration of nucleated gastrin cells per square millimeter of antral and duodenal surface was determined by light microscopy. The mean number of duodenal gastrin cells in the resected duodenum was 4.8 per cent of the total gastric gastrin cell mass. The concentration of gastrin cells in the antrum was quite variable from one mucosal site to another. The degree of extension of the antral gastritic areas was a major factor influencing the mean concentration value. The total number of gastrin cells in the stomach varied from approximately 7 to 74 million cells. Our data indicate that hyperplasia of gastrin cells cannot be demonstrated by studies performed in small specimens taken for biopsy.

Topics: Cell Count; Duodenal Ulcer; Duodenum; Gastrectomy; Gastrins; Humans; Immunoenzyme Techniques; Peptic Ulcer; Pyloric Antrum

Topics: Adult; Aged; Blood Pressure; Female; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Kidney Failure, Chronic; Lithium; Male; Middle Aged; Pepsin A; Peptic Ulcer; Permeability; Polyethylene Glycols; Renal Dialysis; Uremia

Topics: Anemia, Pernicious; Gastric Juice; Gastrins; Gastrointestinal Diseases; Humans; Intrinsic Factor; Lactates; Methods; Pepsin A; Peptic Ulcer; Vagotomy

Topics: Gastrins; Humans; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Gastric Juice; Gastric Mucosa; Gastrins; Peptic Ulcer; Zollinger-Ellison Syndrome

If recurrent peptic ulceration follows partial gastrectomy with Billroth II reconstruction, retained antrum on the duodenal stump may be the culprit. Moderate hypergastrinemia and a high basal acid output (BAO) to maximal acid output (MAO) ratio on gastric analysis should alert the clinician. Careful filling of the afferent loop on barium meal or technetium 99m scanning may verify the diagnosis. The secretin provocative test may be helpful in distinguishing retained antrum from the Zollinger-Ellison syndrome by eliciting a decrease in serum gastrin levels in patients with retained antrum and an increase in serum gastrin levels in patients with Zollinger-Ellison syndrome.

Topics: Aged; Diagnosis, Differential; Gastrectomy; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Pyloric Antrum; Recurrence; Zollinger-Ellison Syndrome

We investigated the effect of mapped antrectomy with gastroduodenostomy on serum gastrin levels in fasting patients and resting lower esophageal sphincter (LES) pressure. Serum gastrin levels in fasting patients were lower in those who had an antrectomy without vagotomy (P less than .05) as compared to control subjects or patients with antrectomy and vagotomy. Resting LES pressure was similar in patients and controls and was not affected by the presence or absence of vagotomy. These findings suggest that (1) mapped antrectomy and gastroduodenostomy without vagotomy are followed by a decrease in serum gastrin and (2) resting LES pressure is not affected by mapped antrectomy and a decrease in serum gastrin level.

Topics: Adult; Aged; Duodenum; Esophagogastric Junction; Fasting; Female; Follow-Up Studies; Gastrins; Gastrostomy; Humans; Male; Middle Aged; Peptic Ulcer; Pressure; Pyloric Antrum; Rest; Vagotomy

Diagnostic procedures for the measurement of gastric acid secretion and for the differention between several types of hypergastrinemia have been improved during the last years. An intravenous dose-response curve with increasing doses of pentagastrin resulted in 30% higher MAO compared to subcutaneously administered pentagastrin (6 microgram/kg body weight). Food-stimulated gastric acid secretions can be measured by intragastric titration; this method is used mainly in clinical-physiological studies. The different forms of hypergastrinemia may be differentiated by 3 provocation tests: calciuminfusion, secretintest, glucagontest. In atypical cases of Zollinger-Ellison-Syndrome it may be necessary to perform all 3 tests.

Topics: Calcium; Dose-Response Relationship, Drug; Gastric Juice; Gastrins; Glucagon; Humans; Pentagastrin; Peptic Ulcer; Secretin; Stomach Diseases; Zollinger-Ellison Syndrome

Gastric acid secretion basally and in response to intragastric meat extract instillation or to tetragastrin, and circulating gastrin concentration basally and after meat extract stimulation were studied in 67 patients with gastroduodenal ulcer, 30 patients after highly selective vagotomy or selective vagotomy for duodenal ulcer, 12 patients after antrectomy for or gastric ulcer and 10 control subjects. Circulating gastrin concentration increased significantly after meat extract stimulation in control subjects, patients with ulceration and patients after highly selective vagotomy, and acid secretion in each group was increased significantly above basal level. In patients after selective vagotomy, significant increase of circulating gastrin concentration was observed, but it was not associated with significant increase of acid secretion. After antrectomy, neither gastrin nor acid secretion increased significantly after meat extract stimulation. In conclusion, present study suggested that (1) gastric acid secretion in response to intragastric meat extract is chiefly affected by the responsiveness of oxyntic cells and release of antral gastrin and that (2) the presence of the antrum is almost essential for acid secretion after a test meal, and release of duodenal gastrin after antrectomy would not be so potent biologically as to result in an acid secretion.

Topics: Adult; Duodenal Ulcer; Eating; Gastric Juice; Gastrins; Humans; Meat; Middle Aged; Peptic Ulcer; Pyloric Antrum; Stomach Ulcer; Vagotomy

Topics: Adult; Cholecystitis; Chronic Disease; Duodenal Obstruction; Female; Gastrins; Humans; Male; Middle Aged; Pancreatitis; Peptic Ulcer

Topics: Animals; Gastric Mucosa; Gastrins; Male; Peptic Ulcer; Rats; Serotonin

Topics: Adult; Aged; Drainage; Female; Gastrectomy; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Pepsinogens; Peptic Ulcer; Recurrence; Vagotomy

Case report on the successful gastric ulcer treatment of a patient with primary hyperparathyroidism with the H2-receptor antagonist cimetidine. After four weeks of therapy with 0.8 g/d cimetidine stomal ulcerations were seen by x-rays and endoscopy to be healed. The patient was discharged on a regimen of 400 mg daily of oral cimetidine. Peptic ulcer did not recur after 1/2 year of treatment with this H2-receptor antagonist, although the signs of primary hyperparathyroidism were still present.

Topics: Aged; Cimetidine; Gastrins; Guanidines; Humans; Hyperparathyroidism; Male; Parathyroid Hormone; Peptic Ulcer

Topics: Electrolytes; Enzymes; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Histamine; Humans; Intrinsic Factor; Pentagastrin; Pepsinogens; Peptic Ulcer; Secretory Rate; Stomach Neoplasms; Vagus Nerve; Zollinger-Ellison Syndrome

Topics: Adult; Cimetidine; Female; Gastrectomy; Gastric Juice; Gastrins; Guanidines; Humans; Peptic Ulcer; Radiography; Zollinger-Ellison Syndrome

Topics: Bombesin; Calcium; Gastrectomy; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Peptides; Pyloric Antrum; Vagotomy

Topics: Duodenal Ulcer; Gastrins; Humans; Peptic Ulcer; Stomach Ulcer

Topics: Adult; Female; Food; Gastric Emptying; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Female; Gastric Mucosa; Gastrins; Humans; Male; Peptic Ulcer; Secretin; Zollinger-Ellison Syndrome

The distribution of parietal cells in the body mucosa, and of G cells in the antral mucosa, was quantitatively mapped in resected stomachs from 42 patients (12 with gastric ulcer, 11 with duodenal ucler, 14 with duodenal ulcer and uremia, and 5 with gastric cancer) who preoperatively had had their gastric acid secretion measured. In the material as a whole there was a significant positive correlation between the parietal-cell density and maximal acid output (MAO), and a significant negative correlation between the parietal-cell density and patient age. A significant positive correlation was found between the antral G-cell mass and basal acid output (BAO). When the individual patient categories were analyzed, the correlation between parietal-cell density and MAO were significant in the group with duodenal ulcer and uremia, and in the group with gastric cancer. Correlation between parietal-cell density and age was found only in the group with duodenal ulcer and uremia. There was no correlation between the parietal-cell density and various parameters of the antral G-cell population in the material as a whole or in any of the individual groups.

Topics: Adult; Aged; Cell Count; Duodenal Ulcer; Female; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Stomach; Stomach Neoplasms; Stomach Ulcer; Uremia

The influence of a coffee-antazid-mixture was investigated at 30 patients with diseases of the stomach (17 with duodenal ulcer, 6 with gastric ulcer and 7 with chronic gastritis) in comparison to a commercial coffee. The parameters measured were the gastric basal acid output, the continuous registration of the pH by an intragastric electrode and the serum gastrin concentration before and after the application of the tests substances. 75% of the patients with duodenal ulcer showed a positive effect by means of a greater elevation of the intragastric pH after application of the mixture in comparison to coffee. The effect was strongly correlated to the basal acid ouptput. In the group with gastric ulcer and that with duodenal ulcer under the influence of the mixture the pH after the initial rise decreased to less deeper values. There was a close relationship to the patterns of gastric ulcer as well with chronic gastritis there was an additional facourable effect on the symptoms of abdominal pain which occured after coffee and not after the mixture. The group with chronic gastritis showed no difference between the pure coffee and the coffee-antacid-mixture. A possible relationship of the products of coffee roasting and the adsorptive properties of the antacid is discussed.

Topics: Adult; Aged; Antacids; Chronic Disease; Coffee; Fasting; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Peptic Ulcer; Stomach Diseases

By arranging a series of psychological contingencies (unpredictability, uncontrollability, conflict), coupled with delivery of a physical stimulus (electric shock), we produced gastroduodenal mucosal lesions in 7 of 8 rhesus monkeys. The most severe conflict paradigm most consistently produced lesions across subjects. Of the 30 lesions observed by endoscopy, 80% occurred near the anatomic junction of gastric body and antrum, in the antrum, or in the duodenum. Lesions varied in severity from discolorations of the mucosa to disruptions of mucosal integrity. Lesions in the stomach generally disappeared in several days despite the continuation of stress; some duodenal lesions were equally evanescent, but in 2 monkeys, lesions lasted over a week. Hydrogen ion kinetics were measured in 2 monkeys that developed gastric lesions and 2 that developed duodenal lesions. The rate at which hydrogen ion entered the duodenum was uniformly suppressed for all 4 monkeys during their first session of shock avoidance; during their last session, the gastric subgroup continued to show suppression while the duodenal subgroup returned towards control levels. Serum gastrin levels were unchanged by the multiple-stress procedures. Our finding of consistently producible, stress-induced gastroduodenal pathology in anatomic areas similar to those involved in man suggests that the subhuman primate is suitable for further efforts to produce an animal model of psychosomatic ulcer disease.

Topics: 17-Hydroxycorticosteroids; Animals; Behavior, Animal; Duodenal Ulcer; Electroshock; Gastric Juice; Gastric Mucosa; Gastrins; Haplorhini; Humans; Hydrogen-Ion Concentration; Intestinal Mucosa; Kinetics; Macaca mulatta; Male; Peptic Ulcer; Stomach Ulcer; Stress, Psychological

Histamine H2-receptor antagonists metiamide and cimetidine were used in the treatment of severe peptic ulceration in Zollinger-Ellison syndrome. The ulcerations were completely healed in all four patients after treatment lasting from six weeks to four-and-a-half-months. Two patients developed recurrent ulcer after the treatment had stopped, but responded to a second course. One patient developed hepatitis B during cimetidine treatment and it is possible that the course of the hepatitis was unfavourable affected by cimetidine. But no other side effects were noted nor was there a significant change in basal serum-gastrin concentration or an increase in H+ secretion. Total gastrectomy remains the treatment of choice in Zollinger-Ellison syndrome, but cimetidine should be considered if the patient refuses operation or operation is not feasible because of a poor general state.

Topics: Adult; Cimetidine; Female; Gastrins; Hepatitis B; Histamine H2 Antagonists; Humans; Male; Metiamide; Peptic Ulcer; Time Factors; Zollinger-Ellison Syndrome

The pathogenesis of peptic ulceration cannot be explained by an abnormal capacity to secrete acid, for ulcers develop in patients who secrete acid normally. Duodenal and gastric ulcers have a common cause. The location of an ulcer in each individual is primarily determined by his capacity to secrete acid at that time. There is a difference between the mechanisms which heal an ulcer and cure a patient of his disease. Procedures that reduce an individual's capacity to secrete acid, heal an ulcer by moving the focus of the ulcerogenic forces to a more proximal site. It is necessary to remove an antral factor if in addition the patient is to be cured of his disease. It is postulated that this antral factor is the gastrin (G17) which is released in abnormal amounts into gastric juice in patients with ulcers and with gastrinomas. The abnormal amount of G17 in gastric juice may be responsible for releasing abnormal amounts of G34 into the circulation from the duodenum and from gastrinomas. The abnormal release of gastrin develops as a result of an impaired response to duodenal acidification manifest in part by an impaired release of secretin. It is postulated that the abnormal stimulation of antral gastrin release may on occasions give rise to antral G-cell hyperplasia, and that the abnormal secretion of gastrin into gastric juice may on occasions give rise to gastrinomas. These abnormalities may cause ulcers by producing an uncontrolled secretion of acid and an abnormal exposure to bile.

Topics: Duodenum; Gastric Juice; Gastrins; Hormones, Ectopic; Humans; Hyperplasia; Paraneoplastic Endocrine Syndromes; Peptic Ulcer; Pyloric Antrum; Stomach Neoplasms; Vagotomy

Topics: Diagnosis, Differential; Diagnostic Errors; Gastrins; Humans; Male; Middle Aged; Pancreatic Neoplasms; Peptic Ulcer; Recurrence; Zollinger-Ellison Syndrome

Topics: Adolescent; Adult; Aged; Anemia, Pernicious; Betazole; Cyclic AMP; Cyclic GMP; Female; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Male; Middle Aged; Pentagastrin; Peptic Ulcer; Stomach Neoplasms; Zollinger-Ellison Syndrome

Topics: Animals; Antacids; Disease Models, Animal; Gastrins; Humans; Peptic Ulcer; Stress, Physiological; Swine

Topics: Animals; Antacids; Disease Models, Animal; Gastrins; Peptic Ulcer; Stress, Physiological

Topics: Gastrins; Humans; Insulin; Peptic Ulcer; Vagotomy

Topics: Gastrins; Gastrointestinal Diseases; Gastrointestinal Hormones; Hormones; Humans; Kidney; Peptic Ulcer; Secretin; Zollinger-Ellison Syndrome

Topics: Dietary Proteins; Gastrins; Gastrointestinal Neoplasms; Humans; Peptic Ulcer; Time Factors

Topics: Adult; Analgesics; Antacids; Female; Gastrectomy; Gastrins; Humans; Hypnotics and Sedatives; Male; Parasympatholytics; Peptic Ulcer; Postoperative Complications; Recurrence; Tranquilizing Agents

Topics: Adolescent; Adult; Aged; Evaluation Studies as Topic; Female; Gastrins; Humans; Japan; Male; Middle Aged; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Chronic Disease; Gastrins; Humans; Liver Diseases; Peptic Ulcer; Prednisone; Stimulation, Chemical

To better define the pathogenetic relationship between gastric acid secretion, serum gastrin levels and acute gastroduodenal disease in burned patients, fasting serum gastrin levels were correlated with the results of a nonaugmented gastric analysis performed in 31 hemodynamically stable burned patients. Gastroduodenoscopy documented the status of the gastric and duodenal mucosa at the time of acid analysis and serum gastrin collection. Twenty-two patients had acute gastroduodenal disease. Dffuse, superficial, gastroduodenal erosions were present in 17 patients; five additional patients had ulcerative lesions. Nine patients had normal endoscopic examinations. Gastrin levels were not predictive of the incidence, severity or location of disease. Gastric acidity, however, did correlate with disease severity-correlation coefficient, r=+0.41,p less than 0.05-being lowest in normal persons, intermediate in superficial disease and highest in ulceration. There was no correlation between the levels of serum gastrin and gastric acid secretion. The relative hyperacidity in patients with acute gastroduodenal disease suggests that acid may be one of the factors potentiating mucosal injury in these patients and may be particularly important in the evolution of life-threatening ulceration.

Topics: Acute Disease; Adolescent; Adult; Burns; Gastric Juice; Gastrins; Humans; Middle Aged; Peptic Ulcer

In 17 patients with postoperative recurrent peptic ulcer, incomplete antrectomy (I.A.) was found by endoscopic biopsies in 5. No evidcence of I.A. was found in the remaining 12 patients. Gastric acid output and gastrin levels were measured in basal conditions and following a calcium I.V. infusion (4 mg/kg hr of Ca++ over 4 hr) and a bombesin (BBS) I.V. infusion (15 ng/kg min over 90 min). Basal gastrin levels were significantly differnt in the two groups of patients: BBS infusion augmented significantly serum gastrin levels in all patients with I.S., while BBS infusion had no significant effect on serum gastrin levels in the group of patients without I.A. Acid output following BBS infusion showed a pattern similar to the pattern seen for gastrin. Calcium infusion augmented gastric acid secretion and gastrin levels in the patients with I.A.; however, the response to calcium could not clearly separate in all instances patients with I.A. from patients without I.A. It is concluded that the "BBS infusion test" may be heplful in the diagnosis of I.A. in patients with postoperative peptic ulcer.

Topics: Adult; Bombesin; Calcium; Female; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Peptides; Pyloric Antrum; Recurrence; Stimulation, Chemical

The effect on serum gastrin levels of lysin-acetylsalicylate (LAS), water soluble derivative of acetylsalicylic acid, was investigated in mice. Intragastrically administered LAS did not at all alter serum gastrin values while--when given via the intravenous route--LAS not earlier than at the very high dose of 450 mug/g caused a short-lived significant increase in serum gastrin. These results are in keeping with the view that salicylates do not owe their potential ulcerogenic properties to stimulation the gastrin-gastric secrection mechanism.

Topics: Animals; Aspirin; Gastrins; Male; Mice; Peptic Ulcer

Until recently in this unit gastroenterostomy was the operation of choice for patients with duodenal ulcer whose maximal acid output (MAO) is less than 30 mmol/hr. Ulceration (jejunal) has recurred in only 2.1%. Unlike partial gastrectomy, which has a peak incidence of ulcer recurrence in the first two years, the incidence of ulcer recurrence remains constant throughout the years after gastroenterostomy. In looking for the explanation of this low recurrence rate we have studied the effect of the operation upon serum gastrin responses to standardized test meals 3 weeks and 26 weeks after operation in 9 patients. Nine normal subjects acted as controls. Six months after operation the responses were significantly lowered, a fall in the serum levels of gastrin at 30, 45, 60 and 90 min after means suggesting that gastroenterostomy reduces both the gastric and intestinal phases of acid secretion. The mean integrated gastrin response (IGR) throughout the postprandial 90 min is also significantly lower 6 months after surgery. The overall mean reduction was 31.1%.

Topics: Adult; Duodenal Ulcer; Female; Gastric Juice; Gastrins; Gastroenterostomy; Humans; Jejunum; Male; Middle Aged; Peptic Ulcer; Recurrence; Time Factors; Ulcer; Wound Healing

Topics: Fasting; Female; Gastrectomy; Gastrins; Humans; Male; Peptic Ulcer; Radioimmunoassay; Stomach Diseases; Stomach Neoplasms

Topics: Duodenal Ulcer; Gastric Juice; Gastrins; Humans; Peptic Ulcer; Pylorus; Recurrence; Stomach Ulcer; Vagotomy

Gastrin is a peptide hormone originating from G-cells of the antrum, the duodenum and the proximal jejunum. From extracts of gastrinomas and from sera of hypergastrinaemic subjects several gastrin molecules could be isolated which were nominated as "mini gastrin" (G13), "little gastrin" (G17), "big gastrin" (G34) and "big big gastrin". Antisera used for radioimmunological gastrin determinations should be characterized with respect to their specificity, as differeing affinity towards the various gastrins and towards CCK-PZ influences the results of the assay and thus the comparability with values of other laboratories. Gastrin is released by direct vagal stimulation of the antral G-cells and by local chemical and physical stimuli in the antrum and duodenum; probably an oxynto-pyloric reflex also exists. Gastrin stimulates in physiologic doses gastric acid secretion and, as shown in dogs and cats, reveals a trophic action on parietal cell growth. H+-secretion and gastrin release are connected by a feed back mechanism, insofar, as a decrease of intragastric pH below 3 inhibits endogenous gastrin release. Hypergastrinaemia has been demonstrated in patients with gastric anacidity or hypo-secretion, benigne pyloric stenosis, uraemia, short bowel-syndrome, gastric and duodenal ulceration and in patients with gastrinomas (Zollinger-Ellison-syndrome). Hypergastrinaemia in combination with hypersecretion exhibits clinical significance in patients suffering from Zollinger-Ellison-syndrome or excluded antrum syndrome which are due to autonomous gastrin release. The differential diagnosis between these syndromes and other diseases, in which hypergastrinaemia is not associated with gastric hypersecretion, can be achieved by several tests using calcium infusion or intravenous application of secretin and glucagon. The significance of elevated gastrin levels in patients with duodenal ulceration (DU) is pointed out. In DU-patients basal and postprandial hypergastrinaemia has been observed. In these patients gastrin release from gastric and extragastric sites is increased. In these patients hypergastrinaemia due to extragastric gastrin release could cause gastric hypersecretion at a time, when the stomach already has emptied. Furthermore parietal cell hyperplasia could be the result of chronic hypergastrinaemia.

Topics: Antibody Formation; Cross Reactions; Gastrins; Humans; Peptic Ulcer; Radioimmunoassay; Zollinger-Ellison Syndrome

Topics: Duodenal Ulcer; Gastrins; Humans; Liver Cirrhosis; Peptic Ulcer

Serum gastrin behaviour after stimulation with a protein meal was examined in 20 patients of both sexes suffering from x-graphically and endoscopically accertained recurring peptic ulcer, and a marked increase was found in the hormone in the majority of patients when observations were made 15 and 45 minutes after the meal. The genesis of this increase is therefore discussed, with consideration of the importance that extra-gastric sites of production of the hormone may have in such penomenon.

Topics: Adult; Female; Gastrectomy; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Postoperative Complications; Recurrence

Topics: Adult; Aged; Female; Food; Gastrins; Gastritis; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Betazole; Gastrins; Histamine; Humans; Peptic Ulcer

Twenty-four patients with postoperative recurrent peptic ulcer, presenting to a teaching hospital over a six-year period, are reviewed. The diagnosis was confirmed by endoscopy or surgery in all cases. Four patients (16-7%) were shown to have the Zollinger-Ellison syndrome and were treated successfully by total gastrectomy. This is a significantly higher incidence of Zollinger-Ellison syndrome than in previous reports. Six patients were treated medically, with one death. In the remainder, an inadequate initial operation was considered to be the cause of recurrence. Reoperation, usually involving complete vagotomy and antrectomy, was performed. There was no mortality in this group, and no patients have had further recurrence. The importance of serum gastrin studies in all patients with recurrent peptic ulcer is emphasized.

Topics: Female; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Postoperative Complications; Recurrence; Zollinger-Ellison Syndrome

Sixty-five patients with peptic ulcer disease were evaluated for gastrinoma (Zollinger-Ellison syndrome) by measuring changes in serum gastrin concentration after intravenous (i.v.) administration of calcium or secretin, or both. The presence of gastrinoma was established in all 20 patients whose serum gastrin increased by 395 pg/ml or more after i.v. calcium and in all 18 patients whose serum gastrin concentration increased by 110 pg/ml or more after i.v. secretin. The experience with these 65 patients shows that stimulation by calcium or secretin may confirm the presence of gastrinoma in cases where the diagnosis would otherwise remain obscure. Although a positive response to calcium or secretin is diagnostic for gastrinoma a negative response does not exclude this diagnosis. Stimulation with secretin is preferred for screening for gastrinoma because it is quicker and more reliable than calcium.

Topics: Adult; Aged; Calcium; Child; False Negative Reactions; False Positive Reactions; Female; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Secretin; Zollinger-Ellison Syndrome

Topics: Duodenal Ulcer; Duodenum; Feedback; Gastrins; Hydrogen-Ion Concentration; Molecular Weight; Peptic Ulcer; Stomach; Stomach Ulcer; Vagotomy; Zollinger-Ellison Syndrome

Histamine H2-receptor antagonists, including burimamide, metiamide and cimetidine, are effective antagonists of histamine-stimulated acid secretion from mammalian, avian or reptilian gastric mucosa. Acid secretion stimulated by gastrin or pentagastrin is also inhibited by these drugs, but there is disagreement about the effects of these drugs on acid secretion resulting from activation of acetylcholine receptors. Based on the pharmacological evidence possibilities of treatment by these drugs were discussed in cases with excessive stimulation of acid secretion due to high blood levels of histamine or gastrin. The positive results in several trials on Zollinger-Ellison syndrome and peptic ulcer were very impressive. Some practical problems have still to be solved, for example the appropriate phase for applying the drugs. The demonstrated clinical effectiveness, however, against peptic ulceration offers a clear alternative to surgery for many patients.

Topics: Burimamide; Gastric Juice; Gastrins; Guanidines; Histamine H2 Antagonists; Humans; Imidazoles; Metiamide; Parasympatholytics; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Antacids; Duodenal Ulcer; Gastric Juice; Gastrins; Gastritis; Histamine Release; Humans; Hydrogen-Ion Concentration; Parasympatholytics; Pentagastrin; Pepsin A; Peptic Ulcer; Stomach Ulcer

Using a 12-hour infusion of salmon synthetic calcitonin (S-CT), distinct and sustained inhibition of gastric acid and pepsin secretion has been demonstrated in 4 normal subjects, 3 patients with peptic ulcer disease and 3 high risk patients. In 3 patients with Zollinger-Ellison syndrome, treated in the same way, elevated serum gastrin was reduced by about 50% and acid secretion by more than 90%. In healthy volunteers oral administration of human synthetic CT (H-CT) led to reduction in basal and pentagastrin-stimulated acid and pepsin secretion by about 50%, lasting for more than 2 hours after the instillation of CT. In 4 subjects receiving CT intravenously, slight nausea and headache were registered, while there were no side effects after the oral route. Serum calcium did not change after i.v. or oral administration of CT. Wheras therapeutical applications of CT, given by i.v. route, seem to be restricted to selected cases, i.e. acute gastric ulcerations with imminent or existent bleeding, the eventual benefit or orally administered CT in peptic ulcer disease should be evaluated in controlled long-term trials.

Topics: Administration, Oral; Calcitonin; Calcium; Gastric Juice; Gastrins; Humans; Injections, Intravenous; Pepsin A; Peptic Ulcer; Stimulation, Chemical; Time Factors; Zollinger-Ellison Syndrome

Topics: Adenoma, Islet Cell; Animals; Dog Diseases; Dogs; Gastrins; Male; Pancreatic Neoplasms; Peptic Ulcer

Twenty-one chronic hemodialysis patients were investigated. While only two had radiologic evidence of peptic ulceration, three had markedly elevated basal acid outputs, thirteen had significantly elevated maximal acid outputs and seven had fasting duodenogastric reflux. Elevated fasting serum gastrin levels and prolonged gastrin circulation following stimulated endogenous release were also demonstrated. The abnormalities in gastric function may be explained by fasting and stimulated hypergastrinemia.

Topics: Adult; Female; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Humans; Hypercalcemia; Kidney Transplantation; Male; Middle Aged; Peptic Ulcer; Renal Dialysis; Uremia

Better knowledge of the physiology of gastric acid secretion and especially the effects of insulin on the secretion, permits better definition of the indications for gastric functional investigation after vagotomy. The most reliable estimation of the effects of vagotomy is obtained by determining, before and after, the basal acid secretion, the maximal and post-insulinic secretions. The results should be expressed as hourly output and not in relation to arbitary criteria based on the titratable acid of the gastric juice. This investigation may be used to determine the quality of vagotomies carried out on a group of patients and to compare series of subjects in which different types of vagotomy were carried out. The tests at present available do not, however, determine precisely the effects of vagotomy in a particular patient. Their use for drawing up individual prognosis has not been demonstrated but their value is far from negligible in the diagnosis of recurrence.

Topics: Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Insulin; Pentagastrin; Pepsin A; Peptic Ulcer; Prognosis; Recurrence; Secretory Rate; Stimulation, Chemical; Vagotomy

Topics: Adenoma; Adult; Aged; Cushing Syndrome; Gastric Juice; Gastrins; Glucagon; Humans; Hypercalcemia; Hyperinsulinism; Islets of Langerhans; Middle Aged; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

An adequate therapy must be directed towards the cause of the recurrent ulcer. This is incomplete vagotomy in most cases, more seldom a hypergastrinemia with stasis in the antrum after insufficient drainage, in hyperparathyroidism, in hyperplasia of the antral G cells or in gastrinoma. After confirmation of the diagnosis by endoscopy, a causal diagnosis must therefore be made which includes secretion analysis and determination of the gastrin profile (feeding test, glucagon provocation test, secretion or calcium infusion). Criteria for evaluation and clinical conclusiveness are shown in examples. The indication scheme, whether revagotomy alone, resection alone or the combination of the two corrective operations should be performed is determined according to these criteria. So far, 41 patients have been operated on with good results in accordance with this graduated indication.

Topics: Gastrectomy; Gastric Juice; Gastrins; Gastroscopy; Glucagon; Humans; Hyperparathyroidism; Insulin; Peptic Ulcer; Recurrence; Vagotomy; Zollinger-Ellison Syndrome

The surgical physiology of the vagus is reviewed with respect to vagotomy in the treatment of duodenal ulcer. All types of vagotomy (truncal, selective gastric, or proximal gastric) produce similar reduction in acid secretion and comparable elevation in serum gastrin. The evidence is mounting that the vagus may have opposing influences on gastrin release: stimulation and inhibition. Division of only the extragastric vagal branches leads to withdrawal of an inhibitory mechanism rendering the denervated stomach more sensitive to the action of gastrin. The loss of this vagally controlled inhibitory mechanism, rather than more meticulous dissection, may explain the higher incidence of more complete vagotomies in selective than in truncal vagotomy. Proximal gastric vagotomy may be the ideal elective operation yet devised for duodenal ulcer. It does, however, cause elevation in serum gastrin and more than 90 per cent of patients after this operation will have positive insulin test in two to four years. This is higher than the positivity seen with truncal vagotomy. Results of controlled trials are needed before this operation becomes fully established.

Topics: Animals; Duodenum; Gallbladder; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hypoglycemia; Liver; Neural Inhibition; Pancreatic Juice; Peptic Ulcer; Stomach; Vagotomy; Vagus Nerve

Serum gastrin and calcitonin were determined after administration of meat extract to patients with peptic ulcer in order to investigate what role gastrin and calcitionin are playing in peptic ulcer. Serum gastrin levels were elevated after ingestion of meat extract in 9 out of 11 patients with peptic ulcer. Serum calcitonin (CT) levels were elevated rather gradually in 7 subjects. It was suggested that increased endogenous gastrin levels may have stimulated the release of CT. When salmon calcitonin (SCT) was admininstered intravenously at a dose of 100 MRCu before administration of meat extract, the rise of gastrin and CT was suppressed in 67% of cases as to gastrin and in 43% as to CT.

Topics: Adult; Aged; Animals; Calcitonin; Eating; Gastrins; Humans; Meat; Middle Aged; Peptic Ulcer; Salmon

Topics: Anemia, Pernicious; Diagnosis, Differential; Duodenal Ulcer; Gastrectomy; Gastric Juice; Gastrins; Humans; Peptic Ulcer; Radioimmunoassay; Recurrence; Zollinger-Ellison Syndrome

The availability of pure intestinal hormones and the development of radioimmunoassays for their measurement has expedited research into many aspects of gastrointestinal endocrinology. A complex balance evidently exists between the different intestinal hormones and also the rest of the endocrine system. Polyendocrinopathies have been described, and, so far, two diseases due to intestinal hormone excess (Zollinger-Ellison syndrome and the syndrome of watery diarrhea, hypokalemia and achlorhydria) elucidated. It seems likely that many more gastrointestinal endocrine diseases await discovery.

Topics: Cholecystokinin; Diagnosis, Differential; Diarrhea; Digestive System; Endocrine Glands; Esophagogastric Junction; Gastrins; Gastrointestinal Hormones; Humans; Hypoglycemia; Intestinal Diseases; Intestine, Large; Pancreas; Peptic Ulcer; Prostaglandins; Pylorus; Secretin; Syndrome; Zollinger-Ellison Syndrome

Topics: Diagnosis, Differential; Gastrins; Humans; Molecular Weight; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Motility; Humans; Peptic Ulcer; Stomach Ulcer

The effect of short-term infusion of a large dose of pentagastrin and a small dose of synthetic human gastrin I (SHG) on the rate of cell proliferation in gastric mucosa was studied in normal human subjects. Moreover, the kinetic parameters were compared with the serum gastrin concentrations in fasting patients. Endoscopic biopsies were labelled in vitro with 3H-thymidine and autoradiographs were prepared. The percentage of DNA-synthesising cells in the progenitor cell region was estimated. In healthy volunteers infusion of a large dose of pentagastrin (10 mug/kg per hour) was followed by a marked increase in the labelling index in fundic mucosa. The antral mucosa was not responsive to this effect. In the same subjects, infusion of a low dose of SHG (8 ng/kg per min) did not affect the rate of cell proliferation, either in fundic or in antral mucosa. In 46 patients with different gastric diseases no correlation between the serum gastrin concentrations and the labelling indices was found. The results suggest that human fundic mucosa is responsive to a trophic action of pentagastrin. If it exists, however, a physiological action of gastrin as a trophic hormone for human gastric mucosa must be considerably more complex than previously believed.

Topics: Adult; Aged; Autoradiography; Cell Division; Female; Gastric Mucosa; Gastrins; Gastritis; Humans; Male; Middle Aged; Pentagastrin; Peptic Ulcer; Stomach Ulcer

Topics: Adult; Gastrins; Gastrointestinal Motility; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Adolescent; Adult; Aged; Female; Gastrins; Gastrointestinal Motility; Humans; Male; Middle Aged; Peptic Ulcer; Stomach

Twenty years of intensive clinical and experimental research have resulted in the successful development of a modern model of gastric secretory and motility physiology as a basis for further differentiating work in this field. Conventional gastric resection as principal method in the treatment of benign hypersecretory gastroduodenal ulcers seems to be superseded by selective proximal vagotomy with pyloroplasty on the basis of excellent results with this procedure. Selective proximal vagotomy can be carried out in place of the standard Billroth resection procedure in 80% of cases. However, the attainment of technical perfection by a few skilled specialist surgeons at selected centres and the precise evaluation of gastric secretion data both pre- and postoperatively are prerequisites for a successful outcome.

Topics: Drainage; Gastrins; Humans; Methods; Peptic Ulcer; Pyloric Antrum; Pylorus; Vagotomy

Topics: Endoscopy; Fiber Optic Technology; Gastrins; Humans; Peptic Ulcer

Based on the data obtained in fibrogastrochromoscopy and histological studies of gastric biopsy specimens from patients with ulcerous gastroduodenal disease, prior to surgical intervention and after gastric resection for this affection, it was found that in "standard" gastric resection with 2/3 of the organ the possibility of remaining a portion of the antral mucous membrane in the gastric stump is practically excluded and, consequently, the role of this factor in the development of peptic ulcer of the anastomosis seems to unliely after the so-called inadquate in extent gastric resections.

Topics: Endocrine Glands; Evaluation Studies as Topic; Female; Gastrectomy; Gastrins; Humans; Male; Peptic Ulcer; Postgastrectomy Syndromes; Pyloric Antrum; Recurrence; Stomach

Topics: Adult; Chronic Disease; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Hepatitis; Humans; Liver; Liver Cirrhosis; Middle Aged; Peptic Ulcer; Stomach Ulcer

Topics: Esophageal Diseases; Esophagogastric Junction; Gastrins; Humans; Peptic Ulcer; Pressure

Topics: Esophagogastric Junction; Gastrins; Humans; Male; Middle Aged; Muscle Contraction; Muscle Relaxation; Peptic Ulcer; Pressure

Gastric secretion was studied in 188 fetuses of 28 pregnant dogs near term. Baseline secretory values were determined and gastric secretion was stimulated in additional fetuses with histamine, insulin, or gastrin. A significant increase in volume, acidity and pepsin output was observed in fetuses stimulated during the last week of gestation. Following maternal stimulation the placental transfer of histamine, insulin, and gastrin are demonstrated.

Topics: Animals; Animals, Newborn; Dogs; Female; Gastric Juice; Gastric Mucosa; Gastrins; Gestational Age; Histamine; Insulin; Peptic Ulcer; Pregnancy; Stimulation, Chemical; Stomach

Patients with recurrent ulcer without retained antrum and with a complete vagotomy will have a low gastric acid output. Those with incomplete vagotomy and gastric resection will have a fasting and histamine-stimulated gastric acid output which are normal' this is as though they had no previous gastric operation. Both groups of patients will have a normal fasting and postprandial serum gastrin. Patients with recurrent ulcer associated with retained antrum will have a fasting and histamine-stimulated acid output above normal. In the latter, fasting serum gastrin will be increased twice normal but not as markedly increased as found in Zollinger-Ellison syndrome. Patients with retained antrum will have a marked postprandial increase in serum gastrin about two times the fasting level. Those patients with this syndrome will have markedly elevated fasting and histamine-stimulated gastric acid as well as marked hypergastrinemia.

Topics: Gastric Acidity Determination; Gastrins; Humans; Peptic Ulcer; Prospective Studies; Recurrence; Surgical Procedures, Operative

Gastric bypass as a 90 per cent gastric exclusion operation was used in 393 patients with massive obesity to limit food intake. Stomal ulcer has occurred in 1.8 per cent of such patients or one ulcer per 140 man years of observation. The studies of indwelling fundic pH and of gastric acid secretion from the excluded stomach indicate that acid secretion is reduced after gastric bypass but that the acid, unbuffered by food in the excluded stomach, results in a lowered gastrin secretion after a meal. Thus, gastric bypass in inhibitory to acid secretion in most morbidly obese patients who do not have known acid peptic disease.

Topics: Achlorhydria; Analysis of Variance; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastroenterostomy; Humans; Obesity; Peptic Ulcer; Stomach Ulcer

Administration of 2-DG accompanied by simultaneous neutralization of gastric contents with sodium bicarbonate resulted in a rise in serum gastrin in 4 patients without gastric disease, 4 with duodenal ulcer and 4 with gastric ulcer. The rise in gastrin equals that observed on stimulation with meat extract. Patients with gastric ulcers display a low PAO and a small rise in gastrin compared with normals and patients with duodenal ulcers. This finding correlates well with the chronic atrophic changes of the antral mucosa in patients with gastric ulcer.

Topics: Bicarbonates; Deoxy Sugars; Deoxyglucose; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Peptic Ulcer; Sodium

Topics: Chronic Disease; Gastrins; Humans; Peptic Ulcer

Topics: Esophagogastric Junction; Fasting; Gastric Juice; Gastrins; Gastrointestinal Hormones; Humans; Peptic Ulcer; Pressure; Stomach Ulcer; Zollinger-Ellison Syndrome

The distributions of acid alpha1-glycoprotein, alpha1-fetoprotein, beta-galactosidase and gastrin in gastric carcinoma and gastric ulcer as well as in the neighbourhood of these lesions were studied by means of immunohistochemical methods on imprint preparation. We could not find significant differences between gastric carcinoma and the nonneoplastic lesions, except for the acid alpha1-glycoprotein. The results of this first study indicate that the immunochemical and immunohistological assay of acid alpha1-glycoprotein might be of practical value in diagnosing malignant changes of gastric mucosa.

Topics: ABO Blood-Group System; alpha-Fetoproteins; Animals; Colonic Neoplasms; Duodenal Ulcer; Fluorescent Antibody Technique; Galactosidases; Gastric Mucosa; Gastrins; Goats; Guinea Pigs; Histocytochemistry; Humans; Peptic Ulcer; Rabbits; Stomach Neoplasms

A retrospective study was made of 34 cases of recurrent ulcer following gastric resection. Males, especially above the age of 40, were shown to be particularly susceptible. The intact vagus apparently plays the most important role in the pathogenesis. Radiological examination and endoscopy are of the greatest diagnostic importance. Truncal vagotomy must be regarded as the treatment of choice in uncomplicated recurrent ulcer. Resection procedures are indicated in perforating ulcer, gastrojejunocolic fistula, antral remains and Zollinger-Ellison syndrome.

Topics: Adult; Duodenal Ulcer; Female; Gastrins; Germany, West; Humans; Male; Middle Aged; Peptic Ulcer; Postgastrectomy Syndromes; Recurrence; Retrospective Studies; Sex Factors; Stomach; Stomach Ulcer; Vagotomy; Zollinger-Ellison Syndrome

Topics: Alkalosis; Antacids; Calcium Carbonate; Carbonates; Drug Interactions; Gastric Juice; Gastrins; Humans; Hypercalcemia; Magnesium Oxide; Parasympatholytics; Pepsin A; Peptic Ulcer; Sodium; Stomach Diseases

Smoking, heredity, aspirin ingestion, and various diseases are associated with increased prevalence of peptic ulcer disease. Significant pathophysiologic differences between ulcer patients and normal subjects have been shown to exist, but many of the observed abnormalities are still poorly understood and require further study. Prospective studies are also needed to quantitate the role of psychologic factors in the pathogenesis of ulcer disease. Ulcer disease is diagnosed by history, physical examination, upper gastrointestinal radiography, and endoscopy. In some patients measurements of serum gastrin levels and gastric acid secretion at rest and after stimulation give significant information. Antacids and anticholinergics remain the primary therapeutic agents; new therapeutic agents are currently under study.

Topics: Antacids; Aspirin; Endoscopy; Gastric Juice; Gastrins; Humans; Parasympatholytics; Peptic Ulcer; Smoking

50 cases of interposition of jejunal loop (32 for gastric cancer and 18 for ulcerous pathology) carried out over the last 3 years are reported. From a technical point of view and as an alternative to degastroenteroanastomosis, interposition of the loop is preferred in partial oral end-to-end on the stomach. In neoplastic lesions, Mouchet-Camey type reconstruction was adopted as a routine measure. After describing the complications of the operation and analyzing the causes, the long-term results are evaluated using absorption curves with 131-I labelled oleic acid. The excellent weight increase in the inflammatory forms, and the lack of reflow and dumping in patients subjected to total gastrectomy for cancer, confirm the value of the technique.

Topics: Adult; Aged; Dumping Syndrome; Duodenal Ulcer; Gastrectomy; Gastrins; Humans; Iodine Radioisotopes; Jejunum; Middle Aged; Neoplasm Metastasis; Oleic Acids; Peptic Ulcer; Postoperative Complications; Radioimmunoassay; Stomach Neoplasms; Stomach Ulcer; Zollinger-Ellison Syndrome

From the experience of treating 91 patients with a proven recurrent ulcer we consider that if a proven ulcer is shown to be present and a gastrin-secreting tumour is excluded an appropriate reoperation will almost always produce a successful result (94 per cent). Before subjecting patients to reoperation all attempts must be made to secure a precise diagnosis. The following investigations should be performed: barium meal, panendoscopy of the upper gastrointestinal tract, determination of maximum acid output (with insulin test and gastrin analysis if appropriate), and cholecystography. Before accepting a diagnosis of recurrent ulcer at least 2 of the first 3 tests should be postive. If the primary operation was a resection we advocate vagotomy alone as the second operation, provided there are no local complications such as stenosis, bleeding, or fistula. If the primary operation was a vagotomy and the recurrence is associated with a positive response to the insulin test we advocate revagotomy and antrectomy. If the insulin test is negative we normally repeat the test; if it is still negative then we use antrectomy alone.

Topics: Barium Sulfate; Cholecystography; Endoscopy; Follow-Up Studies; Gastrectomy; Gastric Acidity Determination; Gastrins; Gastroenterostomy; Humans; Peptic Ulcer; Postoperative Complications; Recurrence; Vagotomy

Topics: Adolescent; Adult; Biopsy, Needle; Chronic Disease; Duodenal Diseases; Gastric Mucosa; Gastrins; Histocytochemistry; Humans; Middle Aged; Peptic Ulcer; Stomach Diseases

Arginine, administered intravenously, was a more potent stimulus to gastrin release than oral Oxo-feeding, while oral arginine failed to elicit a response in normal subjects. Intravenous arginine stimulated a rise in serum gastrin only in normal subjects but not in antrectomized or vagotomized patients. The gastric antrum appears to be the major site of production of heptadecapeptide gastrin and 'mini' gastrin, as measured by the anti-serum used in our radio-immunoassay.

Topics: Administration, Oral; Adult; Aged; Arginine; Chlorides; Female; Gastrectomy; Gastrins; Humans; Injections, Intravenous; Male; Middle Aged; Peptic Ulcer; Peptides; Radioimmunoassay; Stimulation, Chemical; Vagotomy

Topics: Animals; Chromaffin System; Digestive System; Dogs; Endocrine Glands; Enterochromaffin Cells; Gastric Mucosa; Gastrins; Gastritis; Gastrointestinal Diseases; Gastrointestinal Hormones; Humans; Intestinal Mucosa; Intestines; Microscopy, Electron; Peptic Ulcer; Rabbits; Serotonin; Stomach; Zollinger-Ellison Syndrome

Topics: Duodenum; Dyspepsia; Gastric Mucosa; Gastrins; Humans; Intestinal Mucosa; Peptic Ulcer

With better methods of diagnosis, patients will be identified earlier in the course of their disease and will often have atypical and borderline manifestations of the syndrome. Serum gastrin measurements with calcium and especially with secretin challenge will be the most important method of diagnosis. Any patient with acid hypersecretion who has a high serum gastrin level that does higher on secretin infusion should be considered to have the Zollinger-Ellison syndrome. A firm diagnosis of the Zollinger-Ellison syndrome should be made, if at all possible, prior to operation. At operation, a thorough search of the pancreas, duodenum, stomach, greater and lesser omentum and liver should be made for primary and secondary gastrinomas. If the preoperative data firmly establish the diagnosis of the Zollinger-Ellison syndrome, a total gastrectomy should be carried out even if no primary tumor is found. Similarly, a total gastrectomy should be done even if there are massive hepatic metastases. If total gastrectomy is not performed, the patient is apt to die of complications of acid hypersecretion. The only possible exceptions to the rule of always performing a total gastrectomy are in asymptomatic patients with easily excisable tumors or patients with tumors of the duodenum that are easily excisable, providing that in both instances after the excision of the tumor the output of gastric acid as measured at operation is immediately halted. All possible metastatic tumor tissue should be removed. The more tumor tissue removed, the longer the patient will survive. Metastases should be treated aggressively. They do not disappear after total gastrectomy in our experience, and they may kill patients. Patients should be followed after operation with serial measurements of serum gastrin concentrations and by hepatic scintillation scans and hepatic angiography. If hepatic metastases develop, intrahepatic artery infusions of 5-fluorouracil may slow tumor growth.

Topics: Adenocarcinoma; Adult; Aged; Angiography; Calcium; Endoscopy; Female; Gastrectomy; Gastrins; Humans; Lung Neoplasms; Male; Middle Aged; Neoplasm Metastasis; Pancreatic Neoplasms; Peptic Ulcer; Postoperative Complications; Preoperative Care; Radioimmunoassay; Secretin; Zollinger-Ellison Syndrome

Plasma gastrin response to the intravenously administered secretin was investigated in various clinical entities. The marked increase of plasma gastrin was found in response to secretin in a case of suspected Zollinger-Ellison syndrome in contrast to various degrees of plasma gastrin decrease seen in patients with ordinary or postoperative recurrent peptic ulcer. The diagnostic value of secretin provocation test was stressed especially in relation to differentiation between Zollinger-Ellison syndrome and recurrent ulcer due to retained pyloric antrum kept away from the food-passing route, both of which are characterized by hypergastrinemia and acid hypersecretion.

Topics: Adult; Diagnosis, Differential; Gastrins; Humans; Injections, Intravenous; Male; Peptic Ulcer; Postoperative Complications; Recurrence; Secretin; Zollinger-Ellison Syndrome

Whereas 67 patients with duodenal ulcer had fasting and 30-minute postprandial mean serum gastrin levels not substantially different from 32 normal subjects, they had substantially higher fasting and histamine-stimulated gastric acid secretion. The increased acid secretion found in patients with duodenal ulcer is not caused by increased serum gastrin levels. Ten patients with recurrent ulcer, after incomplete vagotomy and gastric resection, had high gastric acid secretion and normal serum gastrin levels. Three patients with recurrent ulcer following complete vagotomy and gastric resection, but with retained antrum, had both high gastric acid secretion and high fasting and postprandial secrum gastrin levels. Three patients with Zollinger-Ellison tumors had even higher basal acid outputs and serum gastrin levels. The combination of basic gastric acid secretory studies and serum gastrin determinations may identify three causes of recurrent ulcer: incomplete vagotomy, retained antrum, and Zollinger-Ellison tumor.

Topics: Duodenal Ulcer; Fasting; Food; Gastric Juice; Gastrins; Histamine; Humans; Peptic Ulcer; Prospective Studies; Pyloric Antrum; Recurrence; Stimulation, Chemical; Stomach Ulcer; Vagotomy; Zollinger-Ellison Syndrome

Topics: Cholecystokinin; Gastrins; Gastrointestinal Hormones; Glucagon; Humans; Intestinal Secretions; Peptic Ulcer; Secretin; Stomach

Topics: Adolescent; Adult; Aged; Depression, Chemical; Female; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Secretin

Topics: Adult; Gastrins; Humans; Male; Peptic Ulcer; Secretin; Zollinger-Ellison Syndrome

In 36 patients with ulcer without Zollinger-Ellison-syndrome (25 patients with recurrent duodenal ulcer, 11 with an ulcus pepticum jejuni after B II-resection of the stomach) and 2 patients suffering from ulcus pepticum jejuni with an ascertained gastrinoma the secretion of acid was compared after stimulation of pentagstrin (6 mug/kg) and calcium (4 mg Ca++/kg/h). The secretion of hydrochloric acid was statistically significantly stimulated in all patients suffering from ulcer by the hypercalcaemia (increase of the serum calcium concentration from 5.0 +/- 0.3 mval/1 to 6.2 +/- 0.8 mval/1). But in patients suffering from ulcer with gastrinoma the stimulatory effect was larger than in such patients without autonomous source of gastrin: the calcium-stimulated secretion of hydrochloric acid was on the average in cases of duodenal ulcer 40% (2 to 68%), in the ulcera peptica jejuni 47% (17 to 75%), in the 4 comparative examinations of the two patients with Zollinger-Ellison-syndrome, however, always more than 100% (106 to 177%) of the pentagastrin-stimulated peak secretion. The comparative test of the pentagastrin and calcium-stimulated secretion of hydrochloric acid could be a help for the proof of autonomous places of the formation of gastrin.

Topics: Acute Disease; Duodenal Ulcer; Gastric Juice; Gastrins; Humans; Hypercalcemia; Jejunum; Peptic Ulcer; Recurrence; Zollinger-Ellison Syndrome

The Exalto-Mann-Williamson procedure produces peptic ulceration in nearly 100% of experimental animals but the mechanism is unknown. To investigate the possible hormonal role of the gastric acid hypersecretion seen after this procedure, we investigated preoperative and postoperative serum gastrin and secretin concentrations. There was no significant change in serum gastrin; however, serum secretin concentrations increased to 2 1/2 times the preoperatve value, most likely secondary to the enhanced secretion of gastric acid. These data do not suppport the theory that alterations in circulating secretin or gastrin levels are responsible for the gastric acid hypersecretion following the Exalto-Mann-Williamson operation.

Topics: Animals; Disease Models, Animal; Dogs; Fasting; Fistula; Gastric Juice; Gastrins; Gastroenterostomy; Jejunum; Peptic Ulcer; Secretin; Stomach

Topics: Gastrins; Humans; Meat; Peptic Ulcer; Recurrence; Stomach Neoplasms

Topics: Gastrins; Gastrointestinal Motility; Humans; Peptic Ulcer; Secretin

Topics: Adult; Gastrins; Humans; Middle Aged; Peptic Ulcer

Topics: Animals; Cattle; Duodenal Ulcer; Fasting; Fluorescent Antibody Technique; Gastrectomy; Gastric Mucosa; Gastrins; Humans; Hyperplasia; Male; Meat; Peptic Ulcer; Pyloric Antrum; Radioimmunoassay; Recurrence; Tissue Extracts

Topics: Administration, Oral; Adult; Aged; Antibodies; Antigens; Arthritis, Rheumatoid; Carbon Dioxide; Chlorides; Female; Gastrins; Glycyrrhiza; Humans; Male; Middle Aged; Peptic Ulcer; Plants, Medicinal; Potassium; Radioimmunoassay; Secretin; Sodium; Succinates; Triterpenes

Topics: Biopsy; Duodenal Ulcer; Gastric Juice; Gastrins; Humans; Hyperplasia; Meat; Peptic Ulcer; Postoperative Complications; Pyloric Antrum; Radioimmunoassay; Recurrence; Tissue Extracts; Zollinger-Ellison Syndrome

Topics: Gastrins; Humans; Hyperplasia; Peptic Ulcer; Pyloric Antrum; Radioimmunoassay; Recurrence; Stomach Ulcer; Terminology as Topic; Zollinger-Ellison Syndrome

Topics: Alcoholic Beverages; Diet; Duodenal Ulcer; Gastric Juice; Gastrins; Gastrointestinal Hormones; Histamine Release; Humans; Indomethacin; Peptic Ulcer; Salicylates; Secretin; Smoking; Stomach Ulcer; Stress, Psychological; Vagus Nerve

Topics: Adolescent; Adult; Aged; Duodenal Ulcer; Female; Gastric Juice; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Middle Aged; Peptic Ulcer; Radioimmunoassay; Secretory Rate; Specimen Handling; Stomach Ulcer

Topics: Duodenal Ulcer; Gastrins; Gastritis; Histamine H1 Antagonists; Humans; Metoclopramide; Peptic Ulcer; Pyloric Antrum; Stomach Ulcer; Vagotomy

Topics: Adenoma, Islet Cell; Adolescent; Adult; Age Factors; Calcium; Child; Fasting; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Humans; Hyperparathyroidism; Male; Middle Aged; Multiple Endocrine Neoplasia; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Gastric Mucosa; Gastrins; Humans; Multiple Endocrine Neoplasia; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Animals; Benzodiazepinones; Carbachol; Cysteamine; Dose-Response Relationship, Drug; Duodenal Ulcer; Gastrins; Peptic Ulcer; Piperazines; Rats; Swine

Topics: Adenoma, Islet Cell; Adult; Aged; Carcinoid Tumor; Diarrhea; Female; Gastrins; Humans; Liver Neoplasms; Male; Microscopy, Electron; Middle Aged; Neoplasm Metastasis; Pancreas; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Gastrectomy; Gastrins; Gastroscopy; Humans; Jejunum; Peptic Ulcer; Postgastrectomy Syndromes; Pyloric Antrum; Radiography; Secretin; Zollinger-Ellison Syndrome

Topics: Digestion; Gastrins; Gastritis; Heart; Hormones, Ectopic; Humans; Peptic Ulcer; Structure-Activity Relationship; Zollinger-Ellison Syndrome

Topics: Administration, Oral; Animals; Calcitonin; Fasting; Female; Gastric Juice; Gastrins; Hydrochloric Acid; Injections, Subcutaneous; Male; Peptic Ulcer; Rats; Swine; Time Factors

In both normal volunteers and in patients with primary hyperparathyroidism, the induction of a metabolic alkalosis by infusion of sodium bicarbonate results in a decrease in serum calcium ion and in an increase of circulating parathyroid hormone concentrations. Bicarbonate infusion may serve in man as a new provocative test for release of parathyroid hormone. Furthermore, we speculate that the metabolic alkalosis which is found at times in patients with the Zollinger-Ellison syndrome and severe peptic ulcer disease may result in parathyroid gland stimulation.

Topics: Adult; Aged; Alkalosis; Bicarbonates; Calcium; Female; Gastric Juice; Gastrins; Humans; Hypercalcemia; Hyperparathyroidism; Male; Metabolic Clearance Rate; Middle Aged; Pancreatic Neoplasms; Parathyroid Hormone; Peptic Ulcer; Sodium Chloride; Zollinger-Ellison Syndrome

Topics: Achlorhydria; Diagnosis, Differential; Duodenal Ulcer; Fasting; Gastrectomy; Gastrins; Humans; Hyperplasia; Malabsorption Syndromes; Male; Middle Aged; Pancreatic Neoplasms; Peptic Ulcer; Stomach Diseases; Zollinger-Ellison Syndrome

Topics: Animals; Diarrhea; Dogs; Dumping Syndrome; Gastric Juice; Gastrins; Gastrointestinal Motility; Humans; Insulin; Peptic Ulcer; Peptic Ulcer Hemorrhage; Peptic Ulcer Perforation; Postoperative Complications; Pylorus; Rabbits; Recurrence; Secretory Rate; Stomach; Vagotomy

Topics: Adult; Cardia; Contrast Media; Dumping Syndrome; Duodenal Ulcer; Esophagoscopy; Esophagus; Female; Follow-Up Studies; Gastrins; Gastroesophageal Reflux; Hernia, Hiatal; Humans; Male; Manometry; Middle Aged; Peptic Ulcer; Peristalsis; Postgastrectomy Syndromes; Posture; Radiography; Radioimmunoassay; Stomach Neoplasms

Topics: Animals; Body Weight; Calcitonin; Female; Gastric Juice; Gastrins; Immobilization; Lactates; Male; Peptic Ulcer; Swine; Time Factors

Topics: Anemia, Pernicious; Gastric Juice; Gastrins; Gastrointestinal Diseases; Humans; Pentagastrin; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Adolescent; Adult; Aged; Animals; Charcoal; Chromatography, Gel; Fasting; Female; Gastric Juice; Gastrins; Gastrointestinal Diseases; Humans; Immune Sera; Iodine Radioisotopes; Male; Middle Aged; Pentagastrin; Peptic Ulcer; Rabbits; Radioimmunoassay; Secretory Rate; Stimulation, Chemical

Topics: Adult; Age Factors; Aged; Blood Group Antigens; British Columbia; Female; Gastrectomy; Gastric Acidity Determination; Gastrins; Gastroenterostomy; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Peptic Ulcer; Postoperative Complications; Recurrence; Sex Factors; Substance-Related Disorders; Time Factors; Vagotomy

Topics: Adult; Calcium; Duodenal Ulcer; Female; Fluorescent Antibody Technique; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hyperparathyroidism; Male; Middle Aged; Parathyroid Glands; Peptic Ulcer; Radioimmunoassay

Topics: Animals; Colon; Denervation; Dogs; Ethanol; Female; Gastric Fistula; Gastric Juice; Gastric Mucosa; Gastrins; Hyaluronoglucosaminidase; Male; Methods; Peptic Ulcer; Stomach; Transplantation, Autologous

Topics: Calcium; Gastric Juice; Gastrins; Humans; Hypercalcemia; Hyperparathyroidism; Male; Middle Aged; Parathyroid Glands; Peptic Ulcer

Topics: Cholecystokinin; Cholelithiasis; Duodenal Ulcer; Esophageal Achalasia; Gastrins; Gastritis; Gastrointestinal Hormones; Humans; Pancreatic Diseases; Peptic Ulcer; Secretin; Stomach Neoplasms; Stomach Ulcer

Topics: Acromegaly; Anemia, Pernicious; Duodenal Neoplasms; Gastric Mucosa; Gastrins; Humans; Hyperparathyroidism; Pancreatic Neoplasms; Peptic Ulcer; Pyloric Antrum; Time Factors; Zollinger-Ellison Syndrome

Topics: Adult; Calcium; Diagnosis, Differential; Duodenal Ulcer; Female; Gastrectomy; Gastric Acidity Determination; Gastrins; Gastritis; Humans; Infusions, Parenteral; Male; Middle Aged; Peptic Ulcer; Pyloric Stenosis; Radioimmunoassay; Vagotomy; Zollinger-Ellison Syndrome

Topics: Animals; Dogs; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Histamine; Methods; Peptic Ulcer; Pyloric Antrum

Topics: Adult; Antacids; Bicarbonates; Calcium Carbonate; Esophagogastric Junction; Gastrins; Humans; Hydrogen-Ion Concentration; Magnesium; Male; Peptic Ulcer; Pressure; Sodium; Stomach; Time Factors

Although histochemical, immunohistochemical, and electron microscopic methods have led to the identification of a large variety of endocrine cells in the upper gastrointestinal mucosa, no conventional light microscopic technique capable of the simultaneous identification of these cells has been reported. Such a staining method would be of considerable value to the pathologist as the malfunction of the endocrine cells of the gut, which produce numerous digestive hormones and biogenic amines, is closely related to a number of clinical conditions afflicting man. In this work, after testing three different polychrome staining methods, it has been concluded that a slightly modified Herlant's tetrachrome in tissues fixed in Zenker-formol is the procedure of choice. This method allows the distinction of several different cell types in the upper gastrointestinal mucosa of man and dog and permits the easy identification of the gastrin-producing cells on a routine basis. This identification has been confirmed in the case of two patients with gastrin cell hyperplasia, seen by both light and electron microscopy. Herlant's tetrachrome has proven valuable in the screening of human as well as experimental gastrointestinal tissues and it has been found to be very suitable for recognizing gastrin-producing cell hyperplasias. The usefulness of this method is expected to increase with the establishment of further correlations between the light and electron microscopy of the endocrine cells of the gut.

Topics: Adenocarcinoma; Animals; Chromates; Dogs; Duodenal Ulcer; Duodenum; Gastric Mucosa; Gastrins; Humans; Hyperplasia; Intestinal Mucosa; Methods; Microscopy, Electron; Peptic Ulcer; Staining and Labeling; Stomach Neoplasms

Topics: Adult; Barium Sulfate; Gastrins; Hematemesis; Humans; Hyperparathyroidism; Hypertension; Laparotomy; Male; Methyldopa; Multiple Endocrine Neoplasia; Peptic Ulcer; Pituitary Diseases; Zollinger-Ellison Syndrome

Topics: Animals; Diagnosis, Differential; Gastric Juice; Gastrins; Humans; Injections, Intravenous; Islets of Langerhans; Peptic Ulcer; Postgastrectomy Syndromes; Pyloric Antrum; Radionuclide Imaging; Secretin; Technetium; Zollinger-Ellison Syndrome

Topics: Duodenal Ulcer; Gastric Acidity Determination; Gastric Juice; Gastrins; Humans; Pepsin A; Peptic Ulcer; Pyloric Stenosis; Radioimmunoassay; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Gastrins; Humans; Insulin; Pepsin A; Peptic Ulcer; Radioimmunoassay

Topics: Adult; Aged; Duodenal Ulcer; Duodenum; Eating; Female; Gastrectomy; Gastrins; Humans; Iodine Isotopes; Male; Middle Aged; Peptic Ulcer; Radioimmunoassay; Time Factors; Vagotomy

One hundred and fifty patients suspected of having Zollinger-Ellison syndrome were investigated. High plasma gastrin levels were found in 23 and in 16 a diagnosis of Zollinger-Ellison syndrome was confirmed. Measurement of the basal and maximal acid outputs showed that these simpler investigations have considerable value as screening tests for the selection of those patients in whom gastrin studies are indicated.

Topics: Gastric Juice; Gastrins; Histamine; Humans; Pentagastrin; Peptic Ulcer; Radioimmunoassay; Secretory Rate; Zollinger-Ellison Syndrome

Topics: Gastric Juice; Gastrins; Humans; Insulin; Meat; Peptic Ulcer; Radioimmunoassay; Recurrence; Vagotomy

Topics: Adult; Esophagogastric Junction; Female; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Manometry; Middle Aged; Peptic Ulcer; Pylorus; Vagotomy

Topics: Administration, Oral; Antacids; Calcium Carbonate; Gastric Juice; Gastrins; Humans; Peptic Ulcer; Stimulation, Chemical

Topics: Adolescent; Adult; Aged; Burns; Child; Child, Preschool; Female; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Animals; Cholecystokinin; Duodenal Ulcer; Eating; Electric Stimulation; Gastric Juice; Gastrins; Gastrointestinal Hormones; Humans; Hydrogen-Ion Concentration; Parasympatholytics; Peptic Ulcer; Pyloric Antrum; Radioimmunoassay; Secretin; Secretory Rate; Stomach Ulcer; Vagus Nerve; Zollinger-Ellison Syndrome

Topics: Acetamides; Gastric Juice; Gastrins; Humans; Peptic Ulcer; Pyridines; Secretory Rate; Structure-Activity Relationship; Thioacetamide

Topics: Gastrins; Humans; Iodine Radioisotopes; Peptic Ulcer; Radioimmunoassay

Topics: Duodenal Ulcer; Gastrins; Humans; Hyperplasia; Meat; Peptic Ulcer; Pyloric Antrum; Recurrence

Topics: Gastrins; Gastrointestinal Hormones; Humans; Peptic Ulcer

Topics: Acromegaly; Dietary Proteins; Gastrectomy; Gastrins; Gastrointestinal Diseases; Humans; Kidney Diseases; Liver Cirrhosis; Peptic Ulcer; Radioimmunoassay; Stomach Neoplasms

Topics: Biological Assay; Diagnosis, Differential; Gastrectomy; Gastrins; Humans; Hyperplasia; Methods; Peptic Ulcer; Postoperative Care; Zollinger-Ellison Syndrome

Topics: Carcinoid Tumor; Gastric Acidity Determination; Gastric Juice; Gastrins; Hormones, Ectopic; Humans; Intestinal Mucosa; Intestine, Small; Pancreatic Neoplasms; Paraneoplastic Endocrine Syndromes; Peptic Ulcer; Stomach; Zollinger-Ellison Syndrome

Topics: Adolescent; Adult; Central Nervous System; Gastrins; Humans; Male; Military Medicine; Peptic Ulcer; Vietnam; Warfare; Wounds and Injuries

Topics: Animals; Cetacea; Chromatography, Thin Layer; Gastric Juice; Gastrins; Gastrointestinal Hormones; Glycosaminoglycans; Male; Peptic Ulcer; Rats; Secretin; Swine

Topics: Diagnosis, Differential; Gastrectomy; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Pentagastrin; Peptic Ulcer; Pyloric Antrum; Recurrence; Secretin; Secretory Rate; Zollinger-Ellison Syndrome

Topics: Adrenal Cortex Hormones; Gastrins; Humans; Hydrogen-Ion Concentration; Immunosuppression Therapy; Kidney Failure, Chronic; Kidney Transplantation; Peptic Ulcer; Postoperative Complications; Transplantation, Homologous; Uremia

Topics: Biliary Tract; Cholecystokinin; Gastrins; Gastrointestinal Hormones; Humans; Pancreas; Peptic Ulcer; Secretin; Stomach

Topics: Adult; Female; Gastrectomy; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Pentagastrin; Peptic Ulcer; Radioimmunoassay; Stimulation, Chemical

Topics: Duodenal Diseases; Gastrins; Humans; Peptic Ulcer; Pylorus; Stomach Diseases; Vagotomy

Topics: Drainage; Gastrectomy; Gastrins; Gastrointestinal Motility; Humans; Methods; Peptic Ulcer; Vagotomy

Topics: Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hydrogen-Ion Concentration; Liver Cirrhosis; Pentagastrin; Peptic Ulcer; Secretory Rate; Stimulation, Chemical

Topics: Animals; Dogs; Duodenal Ulcer; Gastric Juice; Gastrins; Humans; Peptic Ulcer; Stomach; Vagotomy; Vagus Nerve

Topics: Animals; Calcium; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hyperparathyroidism; Immune Sera; Parathyroid Hormone; Peptic Ulcer; Rabbits; Radioimmunoassay; Serum Albumin, Radio-Iodinated

Topics: Animals; Dogs; Gastric Juice; Gastrins; Histamine; Liver Diseases; Peptic Ulcer

Topics: Animals; Gastric Juice; Gastrins; Peptic Ulcer; Rats

Topics: Animals; Bile; Cats; Ceruletide; Cholecystokinin; Drug Synergism; Duodenal Ulcer; Gastric Acidity Determination; Gastric Fistula; Gastric Juice; Gastrins; Gastrointestinal Hormones; Infusions, Parenteral; Pancreatic Juice; Peptic Ulcer; Peptides

Topics: Adult; Aged; Circadian Rhythm; Cross Reactions; Duodenal Ulcer; Female; Gastrectomy; Gastric Acidity Determination; Gastric Juice; Gastrins; Humans; Immune Sera; Intestinal Obstruction; Iodine Isotopes; Male; Middle Aged; Peptic Ulcer; Peptides; Radioimmunoassay; Stomach; Stomach Ulcer; Time Factors

Basal serum gastrin in 40 patients with benign gastric ulcer was 103 +/- 10.7 pg/ml, a level significantly higher than corresponding estimations in normal subjects and patients with duodenal ulcer. Following stimulation by a protein meal, a mean rise of 124 pg/ml was achieved at 75 minutes and prior atropinization induced a rise of 208 pg/ml at 90 minutes. Insulin hypoglycaemia produced a rise of 63 pg/ml which was not significantly changed with concomitant neutralization of gastric contents. These results suggest that patients with gastric ulcer have higher basal gastrin levels than normal and this is probably related to the lowered antral acidity. In addition, the protein meal and insulin hypoglycaemia responses suggest an increased antral G cell mass and the possibility of additional gastrin release from sites outside the antrum. It is doubtful whether the relative hypergastrinaemia has an aetiological role in gastric ulcer but it may have a role in the maintenance of gastric ulcer.

Topics: Adult; Aged; Atropine; Bicarbonates; Blood Glucose; Dietary Proteins; Female; Gastrins; Humans; Immunoassay; Insulin; Male; Middle Aged; Peptic Ulcer; Stomach Ulcer; Time Factors

Topics: Animals; Atropine; Dogs; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Vagotomy

A perfused rat stomach technique which can detect synthetic human gastrin I in amounts greater than 10 ng and measure by block assay amounts greater than 50 ng was used to study circulating gastrin-like activity in normal subjects, patients with peptic ulcer, and patients with the Zollinger-Ellison syndrome. No detectable activity was found in normal subjects or patients with gastric ulcer before or after meals. No activity was found in the fasting plasma of patients with duodenal ulcer but after meals activity could be detected in duplicate samples in seven of 20 patients. In nine proven cases of the Zollinger-Ellison syndrome, gastrin-like activity in the plasma ranged from 15 to 356 ng/ml. The gastrin-like content of two tumours was 6.4 and 29.1 mug/g of tissue. The significance of these findings in relation to immunoassay is described.

Topics: Adult; Aged; Animals; Biological Assay; Duodenal Ulcer; Female; Gastrins; Humans; Male; Methods; Middle Aged; Peptic Ulcer; Rats; Stomach Ulcer; Zollinger-Ellison Syndrome

Topics: Digestive System; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Peptic Ulcer; Regional Blood Flow; Reserpine; Shock, Hemorrhagic

Topics: Gastric Juice; Gastrins; Humans; Peptic Ulcer; Prospective Studies; Pylorus; Stomach; Vagotomy

Topics: Dyspepsia; Gastric Juice; Gastrins; Humans; Peptic Ulcer; Radioimmunoassay; Recurrence; Zollinger-Ellison Syndrome

Topics: Animals; Gastrins; Liver; Liver Cirrhosis; Peptic Ulcer; Rats

Topics: Cholecystokinin; Duodenal Ulcer; Duodenum; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Humans; Intestinal Secretions; Pepsin A; Peptic Ulcer; Secretin; Stomach Ulcer

Topics: Gastric Juice; Gastric Mucosa; Gastrins; Humans; Pepsin A; Peptic Ulcer

Experiments on dogs and rats showed that synthetic human gastrin I was inactivated in the small bowel but not in the liver, whereas pentagastrin was rapidly inactivated by the liver. Similar results were obtained with tissue homogenates. The significance of these results is discussed in relation to the probably increased incidence of peptic ulceration following extensive small-bowel resection in man.

Topics: Animals; Dogs; Gastric Juice; Gastrins; Injections, Intravenous; Intestine, Small; Jugular Veins; Liver; Liver Circulation; Peptic Ulcer; Peptides; Portal Vein; Rats

Topics: Gastrins; Humans; Methods; Peptic Ulcer; Vagotomy

Topics: Anemia, Aplastic; Animals; Antibodies; Chronic Disease; Gastrins; Gastritis; Guinea Pigs; Humans; Liver Diseases; Peptic Ulcer; Rabbits; Radioimmunoassay

Topics: Adult; Deglutition; Deglutition Disorders; Esophagogastric Junction; Esophagus; Female; Gastrins; Humans; Hydrogen-Ion Concentration; Male; Manometry; Middle Aged; Peptic Ulcer; Pressure; Vagotomy

Topics: Animals; Carbon Tetrachloride; Chemical and Drug Induced Liver Injury; Gastric Juice; Gastrins; Liver; Liver Diseases; Liver Function Tests; Male; Peptic Ulcer; Peptides; Rats

Topics: Gastrins; Humans; Peptic Ulcer; Vagotomy

Topics: Adenoma; Adult; Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Male; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Adult; Diagnosis, Differential; Female; Gastric Juice; Gastrins; Humans; Iodine Isotopes; Male; Middle Aged; Peptic Ulcer; Radioimmunoassay; Zollinger-Ellison Syndrome

Topics: Acid-Base Equilibrium; Dietary Proteins; Fasting; Gastrins; Humans; Hydrogen-Ion Concentration; Peptic Ulcer; Radioimmunoassay; Zollinger-Ellison Syndrome

Topics: Animals; Body Weight; Drug Synergism; Gastric Juice; Gastric Mucosa; Gastrins; Male; Nicotine; Pepsin A; Peptic Ulcer; Peptides; Rats; Stimulation, Chemical; Succinates

Topics: Animals; Cats; Cholecystokinin; Depression, Chemical; Dogs; Gastric Juice; Gastrins; Humans; Pepsin A; Peptic Ulcer; Peptides; Pylorus; Secretin; Vagotomy

Topics: Duodenal Ulcer; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Pepsin A; Peptic Ulcer; Stomach Ulcer; Vagus Nerve

Topics: Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastrointestinal Diseases; Humans; Methods; Pepsin A; Peptic Ulcer

The fasting serum level of gastrin was determined by radioimmunoassay in 41 normal subjects, 27 patients with duodenal ulceration, 12 patients with gastric ulceration, and 8 patients following "complete" vagotomy. The patients with duodenal ulceration had significantly higher serum levels of gastrin (1.3 +/- S.D. 0.7 ng./ml.) than normal subjects (0.4 +/- S.D. 0.3 ng./ml.), patients with gastric ulceration (0.4 +/- S.D. 0.4 ng./ml.), or post-vagotomy patients (0.15 +/- S.D. 0.2 ng./ml.).The gastrin secretion in both normal subjects and patients with duodenal ulceration was responsive to protein ingestion, but a larger incremental secretion of gastrin occurred in the latter group. Hyperglycaemia significantly suppressed the serum level of gastrin in both groups. The patients with gastric ulceration had fasting and postprandial serum gastrin levels not significantly different from normal subjects.

Topics: Dietary Proteins; Duodenal Ulcer; Fasting; Food; Gastrins; Humans; Hyperglycemia; Injections, Intravenous; Peptic Ulcer; Radioimmunoassay; Stomach Ulcer; Vagotomy

Topics: Animals; Gastric Acidity Determination; Gastric Juice; Gastrins; Humans; Peptic Ulcer

Topics: Adult; Amino Acid Sequence; Animals; Anura; Cholecystokinin; Female; Gastric Juice; Gastrins; Humans; Intubation, Gastrointestinal; Male; Peptic Ulcer; Peptides; Skin; Stimulation, Chemical; Stomach; Tissue Extracts

Topics: Animals; Anura; Cholecystokinin; Gastrins; Humans; Peptic Ulcer; Peptides; Skin; Tissue Extracts

Topics: Adult; Diet; Female; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Animals; Carbachol; Castration; Estradiol; Female; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Male; Peptic Ulcer; Rats; Secretory Rate; Sex Factors; Stomach

Topics: Amylases; Animals; Cholecystokinin; Chymotrypsin; Digestion; Digestive System; Dogs; Gastrins; Humans; Intestinal Absorption; Lipase; Lipid Metabolism; Pancreas; Peptic Ulcer; Postoperative Complications; Proteins; Secretin; Trypsin; Vagotomy

Topics: Duodenal Ulcer; Gastric Mucosa; Gastrins; Gastrointestinal Hormones; Humans; Hyperparathyroidism; Peptic Ulcer; Stomach Ulcer; Vagotomy; Zollinger-Ellison Syndrome

Topics: Animals; Dogs; Gastric Acidity Determination; Gastric Juice; Gastrins; Histamine; Humans; Peptic Ulcer; Pyrazoles

Topics: Cell Nucleus; Cytoplasmic Granules; Female; Gastrins; Hormones, Ectopic; Humans; Microscopy, Electron; Middle Aged; Pancreas; Peptic Ulcer; Peptic Ulcer Hemorrhage; Staining and Labeling; Zollinger-Ellison Syndrome

Topics: Carbohydrates; Female; Gastric Mucosa; Gastrins; Glycosaminoglycans; Humans; Intubation, Gastrointestinal; Male; Mucus; Peptic Ulcer; Proteins; Pyrroles; Secretory Rate; Stress, Psychological

Topics: Adenoma, Islet Cell; Adult; Animals; Dogs; Female; Gastric Juice; Gastrins; Humans; Male; Pancreatic Neoplasms; Peptic Ulcer; Rats; Swine; Zollinger-Ellison Syndrome

Topics: Animals; Cats; Female; Gastrins; Histamine; Histamine H1 Antagonists; Male; Peptic Ulcer

Topics: Animals; Bicarbonates; Cell Membrane Permeability; Chlorides; Dogs; Dye Dilution Technique; Epithelium; Gastric Juice; Gastric Mucosa; Gastrins; Hydrogen; Mannitol; Osmolar Concentration; Peptic Ulcer; Potassium; Sodium

Topics: Depression, Chemical; Gastric Juice; Gastrins; Humans; Pepsin A; Peptic Ulcer; Peptides; Smoking

Topics: Antacids; Diet Therapy; Duodenal Ulcer; Estrogens; Gastrins; Glycyrrhiza; Humans; Hypothermia, Induced; Male; Parasympatholytics; Pepsin A; Peptic Ulcer; Plants, Medicinal; Stomach; Stomach Ulcer; Terpenes

Topics: Blood Glucose; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Insulin; Methods; Pepsin A; Peptic Ulcer; Proteins; Time Factors; Zollinger-Ellison Syndrome

Topics: Animals; Atmospheric Pressure; Cats; Female; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hypercapnia; Hypoxia; Male; Peptic Ulcer; Peptic Ulcer Hemorrhage; Pulmonary Heart Disease; Pyloric Stenosis

Topics: Biopsy; Diabetes Mellitus; Gastric Juice; Gastric Mucosa; Gastrins; Gastritis; Histamine; Humans; Peptic Ulcer

Topics: Diagnosis, Differential; Gastrectomy; Gastric Juice; Gastrins; Humans; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Gastrins; Humans; Peptic Ulcer

Topics: Animals; Bile; Cats; Duodenum; Gastric Juice; Gastrins; Hydrochloric Acid; Hydrogen-Ion Concentration; Methods; Pancreatic Juice; Peptic Ulcer; Secretory Rate

Topics: Adult; Aged; Amides; Cholecystitis; Dicarboxylic Acids; Female; Gastrins; Gastritis; Gastroenteritis; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Adult; Amides; Dicarboxylic Acids; Gastric Juice; Gastrins; Histamine; Humans; Middle Aged; Peptic Ulcer

Topics: Amides; Dicarboxylic Acids; Gastric Juice; Gastrins; Gastritis; Gastroenteritis; Humans; Peptic Ulcer

Topics: Adult; Aged; Amides; Dicarboxylic Acids; Female; Gastric Juice; Gastrins; Gastritis; Gastroenteritis; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Adult; Amides; Dicarboxylic Acids; Female; Gastrins; Gastritis; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Adult; Amides; Dicarboxylic Acids; Female; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer

Topics: Adult; Aged; Amides; Dicarboxylic Acids; Gastric Juice; Gastrins; Gastritis; Humans; Middle Aged; Peptic Ulcer

Topics: Amides; Animals; Gastrins; Gastrointestinal Diseases; Humans; Intestines; Peptic Ulcer; Rats; Stomach

Topics: Animals; Depression, Chemical; Dogs; Gastric Juice; Gastric Mucosa; Gastrins; Gastroenterostomy; Humans; Intestine, Small; Male; Peptic Ulcer; Pylorus

Topics: Chemical Phenomena; Chemistry; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Hypothalamus; Parasympathomimetics; Peptic Ulcer; Pylorus; Stomach

Topics: Animals; Cats; Female; Gastric Juice; Gastrins; Gastrointestinal Hormones; Male; Peptic Ulcer; Secretin

Topics: Animals; Dogs; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Intestine, Small; Liver Cirrhosis; Peptic Ulcer; Portacaval Shunt, Surgical; Postoperative Complications

Topics: Adult; Age Factors; Aged; Body Weight; Duodenal Ulcer; Female; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Histamine; Humans; Male; Methods; Middle Aged; Peptic Ulcer; Secretory Rate; Sex Factors; Stomach Ulcer; Time Factors; Vagus Nerve

Topics: Animals; Dogs; Gastric Juice; Gastrins; Histamine; Humans; Liver Diseases; Peptic Ulcer; Portacaval Shunt, Surgical

Topics: Achlorhydria; Animals; Bile Ducts; Biliary Tract; Cats; Duodenum; Gastric Acidity Determination; Gastric Juice; Gastrins; Pancreatic Ducts; Peptic Ulcer; Perfusion; Secretory Rate; Time Factors

Topics: Adenoma, Islet Cell; Adult; Carcinoid Tumor; Diagnosis, Differential; Duodenal Neoplasms; Gastric Mucosa; Gastrins; Histamine; Humans; Male; Neoplasms; Peptic Ulcer; Postoperative Complications; Radiography; Serotonin; Tissue Extracts; Zollinger-Ellison Syndrome

Topics: Adenoma, Islet Cell; Adrenal Gland Neoplasms; Adult; Aged; Biological Assay; Female; Gastrectomy; Gastric Acidity Determination; Gastrins; Humans; Hyperinsulinism; Hyperparathyroidism; Male; Middle Aged; Multiple Endocrine Neoplasia; Peptic Ulcer; Pituitary Neoplasms; Radiography; Thyroid Neoplasms; Zollinger-Ellison Syndrome

Topics: Alkalosis; Antacids; Duodenal Ulcer; Gastric Juice; Gastrins; History, 18th Century; History, 19th Century; History, 20th Century; Humans; Pepsin A; Peptic Ulcer

Topics: Adenocarcinoma; Adenoma; Aortography; Diagnosis, Differential; Diarrhea; Gastrectomy; Gastric Juice; Gastrins; Gastrointestinal Hemorrhage; Gastrointestinal Motility; Humans; Hyperplasia; Intestine, Small; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Adolescent; Adult; Aged; Fasting; Female; Gastrins; Humans; Iodine Radioisotopes; Male; Methods; Middle Aged; Peptic Ulcer; Radioimmunoassay; Zollinger-Ellison Syndrome

Topics: Achlorhydria; Anemia, Pernicious; Gastric Acidity Determination; Gastric Mucosa; Gastrins; Histamine; Humans; Peptic Ulcer; Pyrazoles; Stomach Neoplasms; Vagotomy

Topics: Adolescent; Adult; Aged; Female; Gastric Juice; Gastrins; Gastritis; Histamine; Humans; Male; Middle Aged; Peptic Ulcer; Pyrazoles; Stimulation, Chemical

Topics: Animals; Biological Assay; Diagnosis, Differential; Gastric Juice; Gastrins; Humans; Methods; Peptic Ulcer; Peptides; Rats; Zollinger-Ellison Syndrome

Topics: Achlorhydria; Animals; Cats; Duodenum; Gastric Acidity Determination; Gastric Juice; Gastrins; Intestinal Mucosa; Peptic Ulcer; Secretin

Topics: Duodenal Ulcer; Dyspepsia; Gastric Juice; Gastrins; Humans; Peptic Ulcer; Peptides; Stimulation, Chemical

Topics: Adult; Gastric Acidity Determination; Gastrins; Histamine; Humans; Methods; Middle Aged; Peptic Ulcer

Topics: Adult; Blood Transfusion; Duodenal Ulcer; Food; Gastric Juice; Gastrins; Histamine; Humans; Middle Aged; Peptic Ulcer; Secretory Rate; Stomach Ulcer

Topics: Adult; Aged; Animals; Biological Assay; Diarrhea; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Humans; Male; Middle Aged; Pancreatic Neoplasms; Peptic Ulcer; Rats; Secretory Rate; Urine; Zollinger-Ellison Syndrome

Topics: Austria; Gastrins; Humans; Intestinal Secretions; Peptic Ulcer

Topics: Adolescent; Adult; Diagnosis, Differential; Diphenhydramine; Female; Gastric Acidity Determination; Gastric Juice; Gastric Mucosa; Gastrins; Humans; Male; Middle Aged; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Achlorhydria; Anemia, Hypochromic; Anemia, Pernicious; Gastric Mucosa; Gastrins; Humans; Intrinsic Factor; Peptic Ulcer; Peptides; Pylorus; Secretory Rate; Skin Tests; Vagotomy

Topics: Adult; Aged; Female; Gastric Acidity Determination; Gastric Juice; Gastrins; Gastritis; Heart Diseases; Histamine; Humans; Injections, Subcutaneous; Male; Melena; Middle Aged; Neurotic Disorders; Nitrogen; Oral Hemorrhage; Peptic Ulcer; Proteins; Sclerosis; Secretory Rate; Stomach Neoplasms

Topics: Calcium; Gastrectomy; Gastric Juice; Gastrins; Histamine; Humans; Magnesium; Pancreas; Peptic Ulcer; Potassium; Vagus Nerve

Topics: Animals; Denervation; Dogs; Gastrins; Peptic Ulcer; Stomach

Topics: Animals; Dogs; Gastric Juice; Gastrins; Peptic Ulcer; Vagotomy

Topics: Duodenal Ulcer; Gastrins; Hemorrhage; Humans; Peptic Ulcer; Pyloric Stenosis; Stomach Ulcer; Vagotomy

Topics: Animals; Calcium; Dogs; Gastric Acidity Determination; Gastric Juice; Gastrins; Histamine; Hypercalcemia; Hyperparathyroidism; Peptic Ulcer; Secretory Rate; Stomach

Topics: Endocrine System Diseases; Gastric Mucosa; Gastrins; Humans; Peptic Ulcer; Pharmacology; Stomach Ulcer; Surgical Procedures, Operative; Vagotomy; Zollinger-Ellison Syndrome

Topics: Animals; Dogs; Gastrins; Liver Cirrhosis; Liver Cirrhosis, Experimental; Liver Diseases; Peptic Ulcer; Physiology; Ulcer

Topics: Gastric Juice; Gastrins; Gastrointestinal Hormones; Histamine; Humans; Insulin; Peptic Ulcer; Secretin; Serotonin

Topics: Animals; Dogs; Gastrectomy; Gastric Juice; Gastrins; Gastroenterostomy; Gastrointestinal Tract; Humans; Peptic Ulcer; Physiology; Vagotomy; Vagus Nerve

Topics: Duodenum; Gastrectomy; Gastric Juice; Gastrins; Gastrointestinal Hormones; Histamine; Humans; Pancreatic Juice; Peptic Ulcer; Physiology; Radiography; Stomach; Surgical Procedures, Operative; Vagotomy

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Antacids; Diet; Diet Therapy; Gastric Acidity Determination; Gastrins; Humans; Parasympatholytics; Pepsin A; Peptic Ulcer; Physiology; Vagus Nerve

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Alcoholism; Aspirin; Blood Circulation; Body Constitution; Endocrinology; Gastrins; Genetics, Medical; Humans; Infections; Pepsin A; Peptic Ulcer; Phenylbutazone; Psychosomatic Medicine; Research; Stress, Physiological; Toxicology; Tuberculosis; Tuberculosis, Pulmonary

Topics: Adrenal Glands; Autonomic Nervous System Diseases; Gastric Juice; Gastrins; Humans; Metabolism; Nutritional Physiological Phenomena; Nutritional Sciences; Peptic Ulcer; Physiology; Pituitary Gland; Psychology

Topics: Adenoma; Adenoma, Islet Cell; Gastrins; Hormones; Humans; Neoplasm Metastasis; Neoplasms, Multiple Primary; Pancreas; Pancreatic Neoplasms; Peptic Ulcer

Topics: Animals; Dogs; Gastrins; Liver Cirrhosis; Liver Cirrhosis, Experimental; Peptic Ulcer; Research

Topics: Animals; Cats; Dogs; Gastric Juice; Gastrins; Histamine; Peptic Ulcer; Physiology; Pylorus; Research; Vagus Nerve

Topics: Adenoma, Islet Cell; Carcinoma, Islet Cell; Gastrins; Humans; Pancreatic Neoplasms; Peptic Ulcer; Stomach; Zollinger-Ellison Syndrome

Topics: Duodenal Ulcer; Gastrins; Gastrointestinal Hormones; Humans; Peptic Ulcer

Topics: Adenoma, Islet Cell; Gastric Juice; Gastrins; Gastrointestinal Hormones; Humans; Neoplasms; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Anesthetics; Anesthetics, Local; Gastrins; Peptic Ulcer; Ulcer

Topics: Adenoma, Islet Cell; Black People; Gastric Juice; Gastrins; Gastrointestinal Hormones; Humans; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome

Topics: Adenoma, Islet Cell; Endocrine Glands; Endocrine System Diseases; Gastrins; Gastrointestinal Hormones; Humans; Pancreatic Neoplasms; Peptic Ulcer; Ulcer

Topics: Gastrins; Gastrointestinal Hormones; Humans; Peptic Ulcer

Topics: Adenoma, Islet Cell; Gastric Juice; Gastrins; Gastrointestinal Hormones; Humans; Pancreatic Neoplasms; Peptic Ulcer; Zollinger-Ellison Syndrome